Differential diagnosis of glomerulonephritis
in children.
Emergency aid in acute renal failure.
Glomerulonephritis.
Glomerulonephritis is an inflammatory infectious-allergic bilateral disease of kidneys with a primary lesion of glomeruli.
This illustration shows the “nephron” which is the functional unit of the kidney. The kidneys have thousands upon thousands of these and they serve to filter the blood, add in toxins to get rid of, and balance the blood’s electrolytes and pH by adding and subtracting salts. The round tuft-like structure at the head of the nephron is the “glomerulus,” where blood is filtered.
The delicate membranes of the glomerulus, allow salts and very small molecules to pass through while cells and large molecules (like proteins) stay in the blood. Later areas in the nephron balance the salts and small molecules to make sure we keep and dump them in appropriate amounts but the glomerulus is the filter that allows our body’s blood proteins to be conserved. Let’s take a closer look:
The glomerulus is the microscopic kidney area that separates urine from blood. Blood comes in the afferent arteriole, is filtered in a tuft of capillaries, and then exits through the efferent arteriole. The fluid that has been separated out is channeled into the tubules of the nephron for further treatment. Let us emphasize that the filteration membranes are very delicate.
When glomerular disease exists, holes are punched out in this filtration system allowing large molecules (like the proteins that one’s body needs to keep) to enter the urine flow and be urinated away into oblivion.
Acute postinfectious glomerulonephritis is the general term for all cases of inflammation of the filtering units of the kidney following an infection. Up until the mid-1960s, chronic glomerulonephritis was the most common form of chronic renal failure. Thought to be caused by unresolved acute glomerulonephritis, there is no successful treatment for the chronic form of this disease.
Glomerulonephritis (GN) is a non-specific inflammatory disease of the renal glomeruli of immunologic origin. Most forms appear to be brought about by the presence of immune complexes in the walls of the glomerular capillaries with activation of complement and initiation of an inflammatory reaction. It has been generally accepted that soluble immune complexes become deposited in the glomeruli, but over the last few years evidence has been produced to suggest that circulating antibody reacts with antigen at fixed sites in the glomerular capillary wall. The other main immunologic mechanism is the activation of complement by antiglomerular basement membrane antibody fixing on to glomerular capillary walls. This mechanism is rare compared with the immune complex mechanism. Immunofluorescence techniques are used to demonstrate immunoglobulins (antibody) and complement – give a granular pattern outlining the glomerular capillary walls in the immune complex type, and an uninterrupted linear pattern along the capillaries in the antiglomerular basement membrane antibody type.
There is great variety in the morphologic expression of immunologic injury, and the existence of different histologic types form the basis of our classification of g-n. In most of these types all the glomeruli are affected – diffuse g-n; but in others only certain glomeruli are involved -focal g-n. In the focal forms, almost invariably of immune complex type, the complexes are usually confined to mesangial regions and the immunofluorescence pattern reflects this distribution. Glomerulonephritis is the main disease responsible for the end-stage kidneys seen in patients on chronic dialysis and in those requiring transplantation. Much of our present knowledge comes from experimental studies and from the application of immunofluorescence and electron microscopy to material obtained by percutaneous or open renal biopsy.
Etiology:
a) Bacterial (Group A streptococci, staphylococcal) infection
b) Viral ( hepatitis B, mononucleosis)
c) Fungal ( histoplasmosis)
d) Parasitic (toxoplasmosis)
Classification:
Acute glomerulonephritis.
I a) with nephritic syndrome – renal edema, arterial hypertension, hematuria, proteinuria;
b) with nephrotic syndrome – marked edema, high proteinuria ( 3 gr per day and more ), hypoproteinemia, blood cholesterol is increased;
c) with nephrotic syndrome, adding arterial hypertension, hematuria;
d) with urinary syndrome
II Renal function : normal, damaged, acute renal insufficiency.
Chronic glomerulonephritis.
a) nephrotic form – marked edema, high proteinuria ( 3 gr per day and more ), hypoproteinemia, blood cholesterol is increased;
b) hematuric form – hematuria with proteinuria;
c) mixed form – edema, hypertension, and urinary syndroms.
II Renal function : normal Damaged Chronic renal insufficiency
Activity of renal process
Period of exacerbation
Period of partial remission
Period of full clinical and laboratory remission
Subacute (malignant) glomerulonephritis
-Without disorders of renal function
-With disorders of renal function
-Chronic renal insufficiency
Membranoproliferative glomerulonephritis encompasses at least 3 types of chronic nephritis – type I ( with subendotelial deposits ); type II ( with dense intramembranous deposits ); type III (with scattered deposits in the basement membrane).
Type I membranoproliferative glomerulonephritis
Several different morphological patterns can be observed
The “classic” form is characterized by massive mesangial proliferation, mesangial matrix expansion and diffuse thickening of the glomerular basement membrane.
Type II membranoproliferative glomerulonephritis
Dense deposit disease, light microscopy patterns.
(a) Membranoproliferative dense deposit disease pattern 1: hypercellularity and lobular appearance, 400 PAS.
(b) Mesangial proliferative dense deposit disease pattern 2 mild mesangial cell and matrix increase, 400 PAS.
(c) Crescentic dense deposit disease pattern 3 cellular crescent, 400 PAS.
(d) Acute proliferative and exudative dense deposit disease pattern 4 diffuse endocapillary proliferation with numerous macrophages and neutrophils 400 PAS.
Type III membranoproliferative glomerulonephritis with scattered
deposits in the basement membrane.
“Proliferative” – due to proliferation of endothelial cells and mesangial cells.
The mechanism of poststreptococcal acute diffuse proliferative glomerulonephritis is immune : granular deposits of IgG and C3 (“humps”) on the external (subepithelial) side of the basement glomerular membrane. These humps can be seen in electron microscopy and immunofluorescence microscopy.
Acute postinfectious diffuse proliferative glomerulonephritis. Almost all glomeruli are enlarged (hypercellular) due to proliferation of endothelial cells and mesangial cells, swelling of endothelial cells and inflammatory infiltrate (neutrophils and monocytes). This will result in compression of capillaries and Bowman space, which is reduced in size. Initially, tubules are not affected, but with evolution, they may present hydropic change. (H&E, ob. x10)
Chronic glomerulonephritis
Chronic glomerulonephritis represents the end-stage of all glomerulonephritis with unfavorable evolution. This general (glomerular, vascular and interstitial) affection constitutes the so-called “end stage kidney”. In most cases, it is associated with systemic hypertension.
Chronic glomerulonephritis. The majority of the glomeruli are affected. Depending on the stage of the disease, they may present different degrees of hyalinization (hyalinosclerosis – total replacement of glomeruli and Bowmann’s space with hyaline). The hyaline is an amorphous material, pink, homogenous, resulted from combination of plasma proteins, increased mesangial matrix and collagen. Totally hyalinised glomeruli are atrophic (smaller), lacking capillaries, hence these glomeruli are non-functional. Few glomeruli may still present changes which permit to discern the etiology of chronic glomerulonephritis. Obstruction of blood flow will produce secondary tubular atrophy, interstitial fibrosis and thickening of the arterial wall by hyaline deposits. In the interstitium is present an abundant inflammatory infiltrate (mostly with lymphocytes). (Hematoxylin-eosine, ob. x20)
Chronic glomerulonephritis. Functional nephrons have dilated tubules, often with hyaline casts in the lumens. (Hematoxylin-eosine, ob. x20)
Type II Membranoproliferative Glomerulonephritis, (Dense Deposit Disease)
Type II membranoproliferative glomerulonephritis (dense deposit disease) is a rare disease.
Compares the H&E histology of type II MPGN to a normal glomerulus. As with type I MPGN, in this specimen there is hypercellularity and thickening of capillary walls. Some patients with this rare disease have thick capillary walls but no hypercellularity. In that setting, descriptively, membranoproliferative glomerulonephritis isn’t very appropriate, which is why some nephropathologists prefer the term dense deposit disease (DDD). The PAS(on left) and H&E-stained sections demonstrates thickening of the basement membrane and capillary wall, respectively.
The diagram illustrates the dense transformation of the basement membrane that causes the thickening.
Clinics
n Extrarenal symptoms
– edema
– arterial hypertension
n Renal symptomes
– oliguria and anuria
– hematuria
– proteinuria (mild, moderate, significant)
– leucocyturia (rare)
– casts (cylinders): hyaline, epithelial, granular, waxy
n Metabolic syndrome
– disorder of water-electrolyte metabolism
– disorder of protein metabolism
– disorder of lipid metabolism
n Diagnosis can generally be established on the basis of the following clinical and laboratory criteria:
n Acute onset
n Edema
n Hematuria with red blood cell casts in the sediment
n Hypertension
n Evidence of antecedent streptococcal infection
n Lowered serum α- globulin concentration
n Spontaneous improvement in a few days or weeks
Plan of examination
n Fool blood count
n Urinanalysis
n Nechepurenko’s test
n Kakovsky-Addis test
n Ambyrze’s test
n Urine culture
n Zimnitskiy’s test
n Biochemical test of blood
– Serum level of electrolytes
– total protein, albumin and globulin level
– cholesterole
– residual nitrogen, blood urea, creatinine
n Creatinine clearance
newborn 40-65 ml/min/1.73 m2
1 yr and older 60-120 ml/min/1.73 m2
n Ultrasonography of kidneys and urinary bladder.
n Excretory urography
Investigations:
Urine Dipstick test: can be done in clinic. It is cheap, re-producible, give the first insight of what’s wrong with the kidney.
The process to analyze the urine is called Urinalysis.
Normal urine: light yellow colour, clear, transparent. Normal urine colour should never be the colour of tea. Sometimes, the yellow colour can be strong colour due to dehydration, Vitamin B and drug Ricampicin, or the yellow colour become colourless if excessive fluid.
Using the colour indicator test strips, dip to the urine for 5seconds, to measure
-the specific gravity of the urine (how concentrated the urine is)
-the pH (whether the urine is acidic, neutral or alkaline)
-the presence of sugar (glucose), ketones, nitrite, red blood cells, white blood cells and protein
– if has glucose: might means you has diabetis mellitus but you don’t know earlier
– if has ketones: usually the manifestation of ketoacidosis which usually related to type 1 Diabetes
– if has protein: this condition called proteinuria. (Usually we won’t have any protein in the urine since protein is molecule, couldn’t pass the basement membrane of glomeruli.) In proteinuria, means the basement membrane is damaged then protein can leak out into Bowman’s capsule and thus into urine.
24hours urine test: the urine is collected for 24consecutive hours: to test the protein and waste products such as urea, nitrogen, creatinine.
Amount of urea and creatinine excreted is used to calculate Glomerular Filtration Rate (GFR). The normal GFR is about 100-140 mL/min in men and 85-115 mL/min in women. As kidney disease progresses, GFR falls.
Blood test: use the blood to look for creatinine and urea in the blood: Creatinine is a breakdown product of normal muscle breakdown. Urea is the waste product of breakdown of protein. The level of these substances rises in the blood as kidney function is abnormal.
Electrolyte levels and acid-base balance:
One of the functions of the kidney is to regulate the blood’s electrolyte level and monitor acid-base balance in the blood. If the kidney cannot do its function properly, it causes imbalance of electrolyte such as potassium, phosphorus and calcium. High potassium (medical term: hyperkalemia) is a big concern.
Ultrasound: In general, kidneys are shrunken in size in chronic kidney disease, although they may be normal or even large in size in cases caused by adult polycystic kidney disease, diabetic nephropathy, and amyloidosis. Ultrasound may also be used to diagnose the presence of any urinary obstruction, kidney stones, and also to assess the blood flow into the kidneys.
Biopsy: A sample of the kidney tissue (biopsy) is sometimes required in cases in which the cause of the kidney disease is unclear. This is usually done as an outpatient procedure (in A&E), though some institutions may require an overnight hospital stay. Usually, a biopsy can be collected with local anasthetia only by introducing a needle through the skin into the kidney.
In renal biopsy, a small sample of kidney tissue is removed with a needle. The test is sometimes used to evaluate a transplanted kidney. It is also used to evaluate an unexplained decrease in kidney function, persistent blood in the urine, or protein in the urine.
Metabolic
VO2/VCO2 Colorimetric measurements
Urine and Feces Collection
Description: The difference in gas concentrations along with flow information is employed to calculate oxygen consumption, carbon dioxide production and respiratory exchange ratio.
Purpose: Measures metabolism respiratory quotient (RER) – the ratio between the carbon dioxide production and the oxygen consumption. It is an indicator of which fuel (carbohydrate or fat) is being metabolized to supply the body with energy.
Acute Post-Streptococcal or Post-Infectious G-N(APS GN)
Etiology: Group A streptococci of both coagulase +ve and coagulase –ve types, pneumococci and various viruses. Majority caused by streptococci. In the case of Group A streptococci certain types have a propensity for causing g-n; these are types 1, 4, 12, and 49.
Pathogenesis: Considered to be one of the best examples of immune complex disease, although streptococcal antigen is very difficult to demonstrate in glomeruli. C3 is activated via classical pathway although alternative pathway activation has been demonstrated by some workers in addition.
Clinical – Post-streptococcal:
Patient presents with dark colored urine caused by presence of rbc’s in urine. There is puffiness of eyelids, especially in morning; breathlessness may be a feature and this is accompanied by elevated venous pressure. There is often a history of a preceding infection such as a sore throat or tonsillitis; usually there is an interval of several days similar to the latent interval in 1-shot bovine serum albumin g-n in the rabbit.
Some cases, particularly epidemic forms, are caused by skin infections. Cultures of suspected sites should be taken and evidence of streptococcal infection such as raised antistreptolysin-O (ASO), antihyaluronidase (AH), antistreptokinase (ASK), antideoxyribonuclease-B (anti-DNAse-B), and antinicotinamide adenine dinucleotidase (anti-NADase) titers should be sought. Blood pressure and serum urea nitrogen are raised, and urine contains protein, red blood cells, and red cell casts Serum complement level is low.
Pathology – Post-streptococcal:
Grossly the kidneys were enlarged with a pale edematous cortex and accentuated vascularity. Microscopically, all glomeruli are affected and show increased numbers of cells, greater than 120 per glomerular section or greater than four cells per mesangial area. The proliferating cells are endothelial, mesangial, and polymorphs. Some mesangial cells are mononuclears of bone marrow origin. Capillary lumens are reduced in caliber. Occasional crescents may be present, but large numbers indicate a more severe form of attack (see crescentic g-n). There are no other striking features except for casts in tubular lumens and variable numbers of interstitial inflammatory cells. Immunofluorescence microscopy reveals a granular pattern for IgG and C3 along the capillary loops. Properdin has been demonstrated in glomeruli in some cases. Electron microscopy reveals electron dense deposits on epithelial side of glomerular basement membrane (humps) and sometimes deposits on the endothelial side. As the disease resolves the hypercellularity of the glomeruli subsides with the mesangial cells being the last to disappear.
Kidney in glomerulonephritis
Clinical Course and Outcome – Post-streptococcal:
Prognosis is excellent in epidemic forms with complete recovery in the great majority of cases. Prognosis in sporadic cases is good in children, but in adults a certain proportion (up to one-third in some series) will have persistent proteinuria and may progress to a chronic form of g-n with chronic renal failure. Figures on long-term prognosis are rather scanty because percutaneous renal biopsy was not done before mid-1950s.
Acute g-n may also occur during course of staphylococcal endocarditis (coagulase +ve staph). Pathologic picture is similar to post-strep g-n. Acute g-n may also be seen with –ve staphylococcal infections in children with ventriculo-atrial shunts – inserted for relief of hydrocephalus – which have become infected. Acute g-n has also been described in association with pneumococcal and meningococcal infections; these forms are rare. Viruses have also been implicated in some instances.
Crescentic G-N (CrGN-RPGN)
Crescentic g-n is so called because there are large numbers of crescents in glomeruli. Also referred to as rapidly progressive g-n or extracapillary g-n.
Etiology: Usually not determined, but a certain small percentage caused by Group A streptococcal.
Pathogenesis: Some are examples of immune complex disease; others are examples of reaction to antiglomerular basement membrane antibody (anti-GBM). Immune complex group includes those of post-streptococcal etiology. Anti-GBM cases show overlap with Goodpasture’s syndrome, a condition in which bleeding into the alveoli of the lung occurs with crescentic glomerulonephritis; it is caused by antibodies to GBM damaging the glomerular capillary walls and alveoli of the lung. Some patients with crescentic g-n have no demonstrable immunoglobulins in the glomeruli and the background for this group is not understood. The possibility of cell-mediated immunity has been raised for some of these cases, while the likelihood that they are a manifestation of polyarteritis has also been entertained.
Clinical:
Patients – children and adults – have a grave illness with hematuria often being the presenting symptom. Others present with oliguria or even anuria and these are common features whether they are the presenting feature or not. Proteinuria may be heavy and some patients may have nephrotic syndrome. The BUN shows progressive elevation and the natural history of the disease is of a progression to death in renal failure over a few months’ period. BP often elevated. Stigmata of a streptococcal infection present in some. Presence of anti-GBM antibody in serum demonstrable in those with this pathogenesis; anti-GBMAb determined by radioimmunoassay.
Blood in urine
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Symptoms: |
What it could be: |
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Fever; bloody, odd-smelling, or cloudy urine; irritability; vomiting; frequent or painful urination; refusal to eat; pain in abdomen or pelvic area, low back pain, or pain under ribs. |
Urinary tract infection |
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Pain in lower back; blood in urine; child may have been hit or kicked in lower back. |
Trauma to kidneys |
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Blood in urine; usually not noticeable to the eye but detected by urinalysis; recurs regularly; runs in the family. |
Benign recurrent familial hematuria |
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Blood in the urine; foamy urine ranging in color from light brown to bright red; painless; may have no other symptoms. More serious cases may involve reduced urination; swelling of hands, ankles, feet, or legs or around eyes; shortness of breath; vomiting; headache; fatigue. |
Glomerulonephritis |
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Blood in urine while child is taking penicillin, a blood-thinning medicine (like warfarin or heparin), a sulfa-containing drug (like sulfamethoxazole), or drugs for cancer treatment (like cyclophosphamide). |
Some medications |
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Blood in urine following an infection, such as a cold or strep throat or a bacterial skin infection, even if child took antibiotics; usually shows up one to three weeks after the infection.
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An immune reaction following an infection |
Pathology:
There is a widespread involvement of the glomeruli which show proliferative and sclerosing changes in the tufts, and crescent formation along the inside of Bowman’s capsule These crescent may become enormous and fill up most of the capsular space; they are mainly formed by proliferation of epithelium lining Bowman’s capsule with some contribution by macrophage-like cells. The stimulus to their formation is thought to be the presence of fibrin in the capsular space. Tubules show varying degrees of atrophy and loss, and the interstitium may be infiltrated by large numbers of inflammatory cells. As the disease progresses the glomerular tufts become solidified and the crescents may undergo fibrosis; tubular loss accompanies glomerular solidification. Intimal thickening of the small arteries occurs in the later stages and may be the consequence of the hypertension which commonly develops.
Immunofluorescence findings are a granular pattern for IgG and C3 along the glomerular capillary walls in the immune complex type, and a linear pattern for IgG in the case of the anti-GBM type. As noted earlier, immunoglobulins are absent from the glomeruli in some cases. Fibrinogen is demonstrable in the crescents irrespective of the pathogenetic type.
Electron microscopy in the immune complex type may show electron dense deposits in relation to the glomerular capillary walls; often these deposits are in the capillary basement membrane. In the anti-GBM antibody type the tufts show no changes except for occasional fractures of the basement membrane. Fibrin may be demonstrable in relation to the crescents in all.
Membranous G-N (MEM GN)
Membranous g-n is the name given to a condition in which there is an increased thickness of the capillary walls of the glomeruli due to an accumulation of deposits on the epithelial side of the glomerular basement membrane. It may occur in several situations such as in systemic lupus erythematosus or associated with gold therapy for rheumatoid arthritis, penicillamine therapy for Wilson’s disease, syphilis, or tumors. Finally, it occurs in a form (the commonest) referred to as idiopathic or primary membranous g-n which will not be described.
Etiology: Unknown in most cases, but there is evidence to incriminate hepatitis B in some.
Pathogenesis: Immune complex pathogenesis, analogous either to chronic serum sickness model in the rabbit or Heymann-Edgington model in the rat; in the latter, tubular epithelium acts as antigen. Claims have been made in man that tubular epithelium acts as an antigen, but most workers have been unable to confirm this. In situ formation of complexes has been shown in some experimental models as opposed to deposition of soluble complexes.
Clinical
Adults mainly are affected but many cases reported in children. Usual presentation is with nephrotic syndrome – heavy proteinuria, lowered serum albumin, edema, raised serum lipid levels, doubly refractile fat bodies in urine. Serum complement levels normal. Blood pressure and BUN normal at first but may rise later. There is poor response to steroids.
Pathology
All glomeruli affected by a diffuse thickening of the capillary walls of the glomeruli. Special staining techniques reveal thickening due to accretion of material on epithelial side of basement membrane. Silver stains reveal “spikes” which are processes of basement membrane projecting out into the accretions (basement membrane stains positively with silver). Tubules show fatty changes in early stages. Foam cells may be found in the interstitium. As the disease progresses the glomeruli become solidified and tubules disappear.
Immunofluorescence shows granular deposition of IgG and C3 along glomerular capillary loops -more prominent than pattern in acute post-streptococcal g-n. Electron microscopy reveals deposits of electron dense material on epithelial side of glomerular basement membrane; there may be outward projections of basement membrane between these deposits. As the disease progresses the deposits become incorporated into the glomerular capillary basement membrane which increases considerably in width. The deposits may eventually disappear giving rise to a moth-eaten appearance of the b.m.
Membranoproliferative G-N (MP GN)
This is often referred to as mesangio-capillary g-n. It is divided up into two types: type 1 or classical form, and type 2 or dense deposit disease.
Etiology: Unknown for both forms.
Pathogenesis: Classical form has many of the features of immune complex disease. Dense deposit disease – some evidence of alternative pathway activation but apart from that little is known.
Clinical:
Similar in both types. May present as a nephrotic syndrome, but red blood cells in urine are more plentiful than in other examples of nephrotic syndrome. Some patients present with a picture nearer to acute g-n, but in these the degree of proteinuria is heavy. Serum complement are low, especially in dense deposit disease (original name of membranoproliferative g-n was persistent hypocomplementemic g-n). C3 nephritic factor present in dense deposit disease. Dense deposit disease sometimes found as part of a disease called partial lipodystrophy. Blood pressure may be elevated in both types.
Pathology : Classical Form
Glomeruli show generalized involvement. Lobular pattern of glomeruli accentuated ). Increased cellularity of mesangial regions of glomeruli. Localized thickening of glomerular capillary walls, which on silver stains two apparent basement membranes. This is referred to as the tramtrack appearance or double contours ). Foam cells commonly seen in interstitium. Tubules show varying degrees of loss or atrophy. Immunofluorescence findings – coarse granular pattern along peripheral capillaries of glomerular tuft, with C3 in particular and sometimes with IgG in addition. Electron microscopy shows much new formation of basement membrane giving rise to the double contours mentioned above. Increased numbers and increased activity of mesangial cells. Subendothelial deposits are seen in glomerular capillary loops.
Pathology : Dense Deposit Disease
Glomeruli show generalized involvement. Increased cellularity of tufts with more generalized thickening of glomerular capillary walls than in classical form. Other constituents of kidney similar to classical form. Immunofluorescence shows C3 (no IgG) in the mesangium and corresponding to deposits seen by EM. Electron microscopy shows extremely dense deposits in glomerular capillary basement membranes. These are ribbon- or ban d-like and involve long stretches of bm. Similar deposits are seen in Bowman’s capsule and in basement membrane of tubules.
Clinical Course and Outcome:
Prognosis is poor in both forms but worse in dense deposit disease. Patients progress to chronic renal failure over period of several years. Response to treatment is poor in both forms, particularly dense deposit disease. Latter has tendency to recur in renal transplants. Cryoglobulinemia may also present with membranoproliferative glomerulonephritis: Coagula are seen in arterioles and capillaries.
Focal GN – Mesangioproliferative G-N (MESPr GN)
Whereas the forms of g-n described above are diffuse, that is, all glomeruli are involved, there exists a type in which only a certaiumber of glomeruli are involved; the others are apparently normal. This is referred to as focal g-n. Further, the affected glomeruli are only affected partially, that is, only 1 to 2 lobules of the tufts are involved; these glomeruli are said to have segmental or local involvement. Focal g-n may be seen in several generalized diseases such as systemic lupus erythematosus (SLE), Schonlein-Henoch syndrome (HSP GN), subacute bacterial endocarditis (SBE GN), polyarteritis, and Goodpasture’s syndrome. These will be described at the appropriate time. However, there are many cases of focal g-n that occur in the absence of these diseases. In the present state of our knowledge this is a motley group with different clinical pictures; however, recurrent attacks of hematuria make up one clinical group that commonly shows a focal g-n. Recent work has enabled one distinct condition to be dissected out from the others from a pathologic point of view. This is referred to as Berger’s disease (after the man who first described it), or as IgA disease which refers to the predominant immunoglobulin found on immunofluorescence.
IgA disease is characterized clinically by recurrent bouts of hematuria – not related to streptococcal infections – accompanied as a rule by minimal proteinuria. Some cases show heavy proteinuria. On renal biopsy there is often a focal glomerulonephritis with certain glomeruli showing segmental proliferative changes by light microscopy and others showing apparently no change. Another pattern is mesangioproliferative g-n (MESPr GN) in which there is a generalized increase in mesangial cells and matrix. By immunofluorescence, IgA and smaller amounts of C3 and IgG are found with mesangial distribution. Early components of complement Clg and C4 are absent suggesting that the alternative pathway of complement activation is involved. The significance of these findings is not clear at the present time. By electron microscopy, deposits are found in the mesangium.
Hereditary Nephritis (Alport’s Syndrome)
This dangerous form of glomerulonephritis occurs in families and appears to be widespread in the country. Both males and females are affected but males have a much worse prognosis and die during early adult life; females fare much better, although a certaiumber will die from renal failure.
The clinical picture is varied but hematuria is the commonest symptom, coming on sometimes in childhood and tending to be recurrent. Proteinuria varies in its severity and some patients may have a nephrotic syndrome. Another feature is deafness of a high frequency type, but this is not always present; in some affected families some of the siblings may have deafness without the renal lesion. The course of those with renal involvement is a gradual development of chronic renal failure, particularly in the affected males. The genetic analysis seems consistent with autosomal dominant inheritance of a pleiotropic gene, with variable penetrance and expressivity.
The pathologic picture in the early stages is a focal form of glomerular involvement in which segmental areas of bland sclerosis occur in the glomeruli. Some cases show a proliferative picture in the glomeruli. Gradually, more and more glomeruli become sclerotic with concomitant tubular loss. Foam cells containing numerous different lipids are found in the interstitium. At one time foam cells were considered to be a specific change; this is not so; foam cells are found in patients with the nephrotic syndrome of various different origins. However, the presence of interstitial foam cells in a patient without the nephrotic syndrome should arouse the suspicion of hereditary nephritis. Another changes of interest in hereditary nephritis is the appearance of the glomerular capillary walls under the electron microscope. This change consists of a splitting of the basement membrane into several layers accompanied by varying numbers of small round dark particles. This change is common in hereditary nephritis. In addition to the morphologic changes described in GBM, recent studies have shown the absence from the GBM of the so-called Goodpasture antigen.
Chronic glomerulonephritis
Chronic glomerulonephritisis the final stage of many different forms of g-n, but often the kidney is so badly damaged that it is impossible to determine the type of g-n that was the forerunner. In particular it is not possible to determine how many cases of chronic g-n were originally acute post-streptococcal g-n.
The kidneys of chronic g-n are reduced in size and have finely granular subcapsular surfaces. They are firm in texture and often have prominent small arteries indicating thickening as a result of hypertension. Hypertension is a feature of chronic g-n. Other clinical features were described in the lecture on renal failure.
Microscopically the glomeruli are solidified either partially or wholly. Tubules show much loss and atrophy, and arteries show intimal thickening. The interstitium shows fine fibrosis and contains variable numbers of inflammatory cells. Immunofluorescence and electron microscopy are not of much help in sorting out the antecedent forms of g-n because the glomeruli are usually too severely damaged to enable specific patterns to be recognized.
NEPHROTIC SYNDROME
Nephrotic Syndrome is a disorder in the human body, wherein large amount of protein leaks from the blood into the urine, due to damaged kidneys. This spill eventually leads to depletion of protein levels in the body, an increase in the levels of lipid and causes edema (swelling of body parts due to excessive accumulation of watery fluid). Although, it can occur at any age, children between the age group of 18 months to 4 years are at a higher risk.
Approximately two in every 10,000 individuals suffer from Nephrotic syndrome. Let’s evaluate the causes, symptoms and treatment for this kidney disorder.
Causes of Nephrotic Syndrome
Nephrotic syndrome is caused due to the damage to the tiny blood vessels present in the kidney, that are designed to filter waste and excess water from the blood. This condition may arise due to various factors like diseases affecting other parts of the body, such as diabetes and mellitus. A person suffering from glomerulonephritis can also experience Nephrotic syndrome. Non-steroidal anti-inflammatory drugs (NSAIDs), which are harmful for the kidneys, can also lead to this disorder. It is also caused due to allergic reactions stimulated by some insect bites. Nephrotic syndrome may also be a hereditary disorder, though, the chances are very small.
Main causes of NS:
1. Glomerulonephritis
Various forms but membranous and membranoproliferative are commonest
2. Lipoid nephrosis (minimal change disease)
3. Focal and segmental glomerular sclerosis and hyalinosis
4. Generalized systemic diseases:
a) Diabetes
b) Amyloid
c) Systemic lupus SLE
d) Schonlein-Henoch syndrome (HSP GN)
5. Miscellaneous.
Symptoms of Nephrotic Syndrome
The symptoms of this disorder vary from person to person, but the most common symptoms include:
Edema: Bloating or swelling of the body due to accumulation of water in excessive amounts. It is experienced by 95% of the patients suffering from this disorder. The swelling may be noticed in the face, feet, hands, abdomen etc.
Hematuria: A condition wherein the patient may loose blood while passing urine.
Oliguria: The quantity of urine a person passes, decreases substantially when he is suffering from this syndrome.
Pleural effusion: The person experiences difficulty in breathing, due to the accumulation of water in the space surrounding the lungs.
High-blood pressure: An individual suffering from this disorder experiences high blood pressure regardless of his age.
Other than these symptoms the patient experiences anorexia or loss of appetite, fatigue and the patient appears pale.
Patients may lose as much as 25g of protein in the urine each day and this has the effect of depleting the amount of albumin (and in some circumstances other proteins) in the blood. The decreased levels of serum albumin interfere with the colloid osmotic pressure and cause a loss of fluid from the capillaries into the subcutaneous tissues. This occurs particularly in the ankles and legs which become swollen due to edema. Effusions of fluid may occur in the peritoneal cavity (ascites) or in the pleural cavities in patients with severe forms of the NS. Serum cholesterol increases and may reach high levels, but not all cases of NS show high serum cholesterol. Various lipids show elevated serum levels, but it is not known why this is so. Doubly refractile fat bodies are found in the urine and probably reflect the fatty changes that take place in the tubular epithelium.
It is important to realize that the NS is not a disease; it is a syndrome caused by many different renal diseases. When a clinician encounters a patient with the NS it is important for him to determine the underlying condition, because the course and prognosis will depend on the underlying disease.
Ascytis and pale skin at NS
Hydrothorax Hydropericardium
There may be brittle and tarnish the hair, skin cracks, from which liquid flows, striae distensae.
Striae distensae
Diagnostic
1. Urine protein exretion is more than 1 g/m2/day; exretion rates of more than 5 g/day are common in young children. Albumin is the principle urinary protein in NS.
2. Hypoalbuminemia (less than 2,5g/dl) is characteristic. Serum levels of alfa-1 globulin are decreased; levels of alfa-2 globulins, beta globulins, and fibrinogen show a relative or absolute increase.
3. Serum levels of cholesterol, tryglycerides, and total lipids are increased, reflecting both increased production and decreased clearance of lipid. Cholesterol levels vary inversely with serum albumin levels.
4. The urine contains hyaline and granular casts, free lipid, cholesterol-containing bodies, and fatty casts. Microscopic hematuria is present in 25 % of children with NS; gross hematuria or red blood cell casts suggests other glomerulara diseases.
5. Serum BUN and cretinin levels are midly increased in 25 % of children with NS, reflecting reduced intravascular volume; the levels normalize with onset of diuresis. Persistent of worsening azotemia suggests other glomerular diseases.
6. Serum complement levels are normal; a decrease suggests membranoproliferative glomerulonephritis or systemic lupus erythematosus. decreased serum levels of Factor B and Ig G may contribute to increased susceptibility to infection, decreased serum antithrombin III and plasminogen to increased risk of thrombosis.
An individual, who shows the symptoms of Nephrotic disorder, is subjected to a blood test and urine test to measure the amount of protein, cholesterol and sugar in the blood. More sophisticated tests like ultrasound, CT scan, and MRI can be performed for accurate detection of the disorder. A biopsy of the kidney can also be helpful in determining the extent of damage suffered by the organ.
COMPLICATION
Nephrotic children are at increased risk of serious bacterial infection (S.pneumoniae, E. coli, H. influenzae), including septicemia, spontaneous peritonotis, urinary tract infections, and cellulitis. Promptly evaluate children with fever, abdominal pain, dysuria, etc. and initiate appropriate antibiotic therapy as indicated. The risk of deep venous and renal vein thrombosis is increased in nephrotic patients, due to their hypercoagulation state.
Treatment
The main methods of treatment of acute glomerulonephritis are regime, diet and medication which are determined by pediatricians, depending on the health of a sick child, treatment may be carried out in hospital or at home. In the acute period it is necessary to prescribe bed regime and warm the child. Bed rest should be observed until recovery of diuresis, reduction of swelling, lower blood pressure and elimination of massive haematuria (usually no more than 3 – 4 weeks).
The basis used diet is to limit the content of sodium in the diet, a temporary restriction of protein and fluid. “Therapy hunger and thirst” should not be applied, because it causes the collapse of the endogenous protein with hyperasotemia. In the first period of the disease salt-free diet must be used. The number of drunken fluid diuresis must exceed the previous day at 400 – 500 ml (to compensate for extrarenal losses). The total caloric content of food must meet the age requirements at the expense of fats and carbohydrates. During the first 4-6 weeks of illness some limitation of protein are desirable (up to 1-1,5g per 1kg body weight per day) with subsequent transition to physiological norms.
In acute glomerulonephritis of the child’s nutritional products, causing allergy and maintaining and strengthening hypertension and edema, are excluded. Products containing potassium must be added in the ration: potatoes, raisins, dried apricots, bananas. Only at renal failure the protein is limited to (1,0-1,5 – 2g / kg) at the expense of meat, fish, cottage cheese.
Smoked meat, strawberries, strawberries are forbidden. Diet expands within 3-4 weeks only if there is stable remission. Duration of diet therapy is 3-6 months.
Primary Glomerulonephritis
Adjuvant therapy:
As supporting therapy a protein diet with 0.6g protein/kgBW/day plus protein amount in the 24 hours-urine (until a maximum 1g protein/kgBW/day) is recommended. A professional dietary advise has to be given to each patient.
Treatment of acute Glomerulonephritis
n Complete bed rest until the symptoms subside.
Diet N 7a (Restriction of proteins, low quantity of fats & carbohydrates, water, salt, allergenic foods) salt
– at the 4-5 week 0.5 g/day
– at the 8 week 1.5 g/day
– for nest 2 yrs 50 mg/kg
n proteins (in case renal failure)
– at the first 1-4 days – 0.5-1g/kg
– 5-7 days – 1-1.5 g/kg
– 7-10 days – 2.5 g/kg
liquid
15 ml/kg (400 ml/m2)
n Antibacterial treatment (for 8-10 days, two cycles)
– BENZYLPENICILLIN Na – 20.000-50.000 U/kg – 7-10 days
– amoxiclav 25-50 mg/kg,
– or cefotaxim 100-150 mg/kg,
– or ceftriaxon 100 mg/kg,
– or ciprophloxacin 10-20 mg/kg per day in 2 equal doses.
– or macropen 30-50 mg/kg
n treatment of chronic locus of infection
n membranostabilizers
– tocoferol acetatis
n Improvement of renal flow
– electrophoresis with nicotinic acid or heparin
– i/v injections of
n euphyllin 2 mg/kg 3 times per day
n trental 5 mg/kg 3 times per day (amp. 5 ml 2 % sol., dragee 100mg) or dipiridamol 5 mg/kg 3 times per day per os
n Vitamin therapy
n Management of edema
– lasix 1-2 mg/kg i/m
– hypothiazid 0.5-1 mg/kg per os
n Management of hypertension and eclampsia
– renin-angiotensin-aldosteron system antagonists
n captopril, cozaar, analapril 0.25-0.5 mg/kg
n in crisis: 0.1 ml/kg of 1% papaverini + 0.1 ml/kg of 0.5 % dibazoli
Depending on the causes of disease and characteristics of clinical course antibiotics may be used. It is advisable to use drugs directed against streptococcal infections – penicillin, semisynthetic penicillins.
It is necessary to treat chronic foci of infection (dental caries, chronic tonsillitis).
Treatment of chronic glomerulonephritis
1. dipiridamol 10 mg/kg 3 times per day per os + Indometacin 1-3 mg/kg
n in case of renal failure
Corticosteroids 2-3 mg/kg/day + cyclosporin A 5-10 mg/kg/day +dipiridamol 5 mg/kg 3 times per day per os
Treatment of subacute glomerulonephritis
1. Corticosteroids 2-3 mg/kg/day + cyclophosphamide 4-5 mg/kg/day or cyclosporin A 5-10 mg/kg/day
2. trental 5 mg/kg 3 times per day or dipiridamol 5 mg/kg 3 times per day per os
3. heparin (fraxiparin) 500 IU/kg/day
4. Plasmapheresis
pulse-therapy
Corticosteroids 20-25 mg/kg/day i/v for 3-6 times
Minimal Change Glomerulonephritis
(MCGN, minimal proliferative intercapillary glomerulonephritis with nephrotic syndrome (MPI + NS), glomerular minimal changes, lipoid nephrosis, minimal change nephrotic syndrome)
Prednisolone: 1 mg/kgBW/d for 6 weeks or until 14 days after positive respond to therapy (24 h Proteinuria <
In the case of non-response or relapse this therapy is repeated in the same way.
In the case of frequent relapse, rebiopsy is advised.
In the case of treatment-failure to Prednisolone or for frequent relapsers, randomization will be performed.
Group A:
Combination therapy with Prednisolone 1 mg/kgBW/d and chlorambucil 0.15 mg/kgBW/d for two weeks, thereafter 0.3 mg/kgBW/d for four weeks in total.
The maximal dose for chlorambucil is 11 mg/kgBW and will be achieved after six weeks.
Group B:
Monotherapy with cyclosporin A 5 mg/kgBW/d; increase dose according to whole blood level within 14 days (to achieve blood levels of 80 -120 ng/dl).
Duration of therapy: 6 months.
Focal-segmental Glomerulonephritis (FSGS)
(Focal-Segmental Glomerulosclerosis)
Group A:
Prednisolone 1.5 mg/kgBW/d po (Dose reduction see group B) plus ASS 500 mg/d
If remission cannot be achieved, cyclosporin A will be given as monotherapy. Start with 3 mg/kgBW/d, increase dose until therapeutical whole blood levels are reached (80 – 120 ng/dl) within two weeks.
Duration of therapy: 6 months
Group B:
Prednisolone 1.5 mg/kgBW/d po for at least two weeks. If there is a positive response decrease dose gradually.
If no treatment response can be obtained within 6 weeks (continued Proteinuria), add (as combination therapy): Chlorambucil 0.1 to 0.4 mg/kgBW/d according to blood counts (absolute lymphocyte count < 1000/l).
Duration of therapy: 6 to maximum 12 weeks.
In this combination therapy the steroids should be given alternatively every second day in the morning.
If no remission is achieved (continued Proteinuria > 1 g/24 h) cyclosporin A should be given as monotherapy: start with 3 mg/kgBW/d, increase dose until therapeutical blood levels of 80 to 120 ng/dl in whole blood.
Duration of therapy: 6 months
Membranous glomerulonephritis
(MGN, peri-membranous glomerulonephritis)
Group A:
The treatment follows the De Santo-Scheme (De Santo et.al., Am.J. Nephrol. 7, 74 – 76, 1987) with a combination therapy of Prednisolone and Cyclosporin A.
Prednisolone: beginning with 1,0 mg/kgBW/d over one week; stepwise reduction to 0,3 mg/kgBW/d until the end of the first month, ongoing dose reduction to 0,15 mg/kgBW/d until the end of the second month, the then achieved dose will be carried on as continuous medication.
Cyclosporin A: slow begin with 3 mg/kgBW/d, dose adaption until a therapeutical concentration of 80 to 120 ng/dl (whole blood) within two weeks.
Duration of therapy: 6 months.
During the treatment period a salt depleted diet has to be ordered; if necessary there should be given additionally diuretics and antihypertensive drugs.
When Proteinuria rises again therapy according to the Ponticelli-scheme (below). Between the two therapies a pause of one month must be kept.
If a second relapse occurs the therapy will be stopped.
Group B:
Cycle A, 1. month:
Methylprednisolone:
Prednisolon: 0,5 mg/kgBW/d po day 4 to 30, dose of Prednisolone should be given in the morning between 7 and 9 o’ clock, no slow reduction on day 30) .
Cyclus B, 2. month:
Chlorambucil: 0,2 mg/kgBW/d po day 1 to 30.
If the leucocyte count falls under 5000/l reduction of the dose. Cycle A and B should be repeated each twice, thereafter dose reduction of the Prednisolone.
Duration of therapy: ca. 6 months.
During this time a salt depleted diet has to be given, if necessary diuretics and antihypertensive drugs have to be prescribed.
In case of relapse: Monotherapy with Cyclosporin A (6 months); slow begin with 3 mg/kgBW/d, dose adaption until a therapeutical concentration of 80 to 120 ng/dl (whole blood) within two weeks.
Group C:
Control group: only symptomatic therapy of the hypertension.
Membranoproliferative glomerulonephritis type I and II (MPGN)
Group A:
The therapy follows the Donadio-scheme (Donadio et.al., N.Engl.J. Med. 410, 1426, 1984)
Dipyridamole: 75 mg/d p.o. as continuous medication
ASS: 500 mg/d po as continuous medication
Mesangioproliferative Glomerulonephritis (MESGN)
There will be a randomization into three groups.
Group A:
Prednisolone: 1 mg/kgBW/d for 6 weeks po or until 14 days after a positive reaction (Proteinuria < 1 g/24 h, thereafter stepwise dose reduction, weekly for 50% until 20 mg/d, then every three days for another 5 mg).
Additional therapy with ACE-Inhibitors:
Enalapril: The dose has to be chosen until normotension is achieved; therefore should a dose until a maximum of 20 mg/d be given.
Duration of therapy: 6 weeks.
If normalization with this medication caot be achieved, enalapril should be given in combination with a diuretic (e.g. fursemide).
Group B:
Prednisolone: 1 mg/kgBW/d for 6 weeks or until 14 days after positive reaction (Proteinuria < 1 g/24 h). Dose reduction as described above.
Therapy without ACE-Inhibitors. Even the possible hypertension should not be treated with ACE-Inhibitors.
Duration of therapy: 6 weeks.
In the case of relapse repeat protocol.
Group C:
Control group: no steroids, no ACE-Inhibitors, symptomatic therapy of the hypertension.
IgA-Nephritis (IgAN)
There will be a randomization into three groups.
Group A:
Indomethacin 100 mg 1 x 1 cpm?./d po
Acetyl-salicyl acid 1 X 100 mg/d po
Duration of therapy: 1 year
Group B:
Prednisolone: 1 mg/kgBW/d for 6 weeks or until 14 days after positive response to therapy (Proteinuria < 1 g/24h). Thereafter stepwise dose reduction (weekly for 50% until 20 mg/d, thereafter every three days for 5 mg).
Group C:
Control group: Symptomatic therapy
Rapid Progressively Glomerulonephritis (RPGN)
RPGN-Type I, Anti-GBM-Disease, linear immunofluorescence
No randomization!
Three fold combination therapy with
1. Plasmapheresis: 40 to 50 ml/kgBW plasma should be exchanged against albumin and fresh frozen plasma (50 to 100 %) during two weeks at least. A minimum of 15 plasmapheresis are to be performed on the patient before effectiveness can be assessed..
2. Modified “pulse therapy” with Prednisolone: 1/2 g iv day 1 to 3: 100 mg po; over one week 80 mg po; over 1 week 40 mg po; then weekly reduction of 5 mg.
3. Cyclophosphamide: beginning with 2 mg/kgBW/d po; dose adaption so that the absolute lymphocyte count lays beneath 1000/l.
Duration of treatment: at least 6 months.
The Cyclophosphamide therapy plus low dosed Prednisolone therapy should be remained for at least 6 month after the end of the signs of activity.
RPGN-Type II, Immune-Complex-Nephritis (granular immunofluorescence)
RPGN-Type III (negative Immunofluorescence)
There will be a randomization into two groups:
Group A:
No plasmapheresis.
Pulse therapy with Prednisolone as by RPGN type I described beginning on day 1 and Cyclophosphamide beginning with 2 mg/kgBW/d po Absolute lymphocyte count < 1000/l; dose adaption according to lymphocyte counts.
Group B:
Modified Euler-Scheme:
Combination therapy with:
1. Plasmapheresis: 3 times, day 1, 2, 3 then
2. Prednisolone pulse therapy from day 1 to 3 (see RPGN type I) every time after plasmapheresis.
3. Cyclophosphamide-therapy after the third plasmapheresis 375 mg/m body surface iv once just after the last plasmapheresis.
Continuation with Cyclophosphamide 2 mg/kgBW/d po for at least 6 months. Absolute lymphocyte count < 1000/l, eventual dose adaption.
If no response is noted after 8-weeks of therapy a rebiopsy should be carried out in all three forms of RPGN. If marked interstitial fibrosis is reported or most of the glomeruli are necrotic the therapy must be stopped and the patient should receive chronic dialysis treatment.
Treatment of Nephrotic syndrome
Treatment of Nephrotic syndrome can be initiated after the exact cause of the disorder is determined. The treatment includes medication and a proper diet, that helps in slowing down or reversing the damage caused to the kidney. The medicaments include giving corticosteroids like prednisolone, to reduce the swelling caused due to the disorder. If corticosteroids don’t improve the condition, then cyclophosphamide or cyclosporine can be given. Diuretics like bumetanide are given to reduce the sodium, potassium and water retention in the body, and angiotensin-converting enzyme (ACE) inhibitors to keep a check on the amount of protein lost while passing urine. Some precautions need to be taken when medications for the treatment for Nephrotic syndrome are administered. Although, diuretics are used to reduce water retention, excessive intake often causes further damage to the kidney. Therefore, medicaments should be taken strictly after consulting the doctor, as improper intake can worsen the situation.
The chances of the occurrence of Nephrotic disorder are very rare, but if the diagnosis and the treatment are not implemented as soon as the symptoms are noticed, then it can lead to major complications such as chronic kidney diseases. After all, a healthy body and a healthy mind are the only way to a happy life.
Acute renal failure (ARF)
Acute renal failure (ARF), also known as acute kidney failure, is a rapid loss of renal function due to damage to the kidneys, resulting in retention of nitrogenous (urea and creatinine) and non-nitrogenous waste products that are normally excreted by the kidney. Depending on the severity and duration of the renal dysfunction, this accumulation is accompanied by metabolic disturbances, such as metabolic acidosis (acidification of the blood) and hyperkalaemia (elevated potassium levels), changes in body fluid balance, and effects on many other organ systems. It can be characterised by oliguria or anuria (decrease or cessation of urine production), although nonoliguric ARF may occur. It is a serious disease and treated as a medical emergency.
History
Before the advancement of modern medicine, acute renal failure might be referred to as uremic poisoning. Uremia was the term used to describe the contamination of the blood with urine. Starting around 1847 this term was used to describe reduced urine output, now known as oliguria, which was thought to be caused by the urine’s mixing with the blood instead of being voided through the urethra. Acute renal failure due to acute tubular necrosis (ATN) was recognised in the 1940s in the
Causes
І. Prerenal:(decreased perfusion).
1. Acute gastroenteritis (vomiting, diarrhea, nasogastric tubes).
2. Acute anemia (hemolytic crises, including sickle cell crisis).
3. Shock.
4. Congestive heart failure
ІІ. Renal:
1. Acute tubular necrosis:
· fluid loss, hemorrhage, shock
· intravascular hemolysis
· sepsis
· nephrotoxic drugs, chemical, radiocontrast substances
· major surgical procedures, road accidents, extensive burns
· hepatic failure, congestive cardiac failure
2. Glomerular diseases:
· acute glomerulonephritis
· hemolitic uremic syndrome
3. Interstitial nephritis.
4. Acute bacterial pyelonephritis.
5. Miscellaneous:
· snakebite
· renal vein thrombosis
ІІІ Post-renal (obstructive): Calculus, blood dots, crystals of uric acid, sulphonamides.
Pre-renal (causes in the blood supply):
· hypovolemia (decreased blood volume), usually from shock or dehydration and fluid loss or excessive diuretics use.
· hepatorenal syndrome in which renal perfusion is compromised in liver failure
· vascular problems, such as atheroembolic disease and renal vein thrombosis (which can occur as a complication of the nephrotic syndrome)
· infection, usually sepsis
· systemic inflammation due to infection
Renal (damage to the kidney itself):
· toxins or medication (e.g. some NSAIDs, aminoglycoside antibiotics, iodinated contrast, lithium, phosphate nephropathy due to bowel preparation for colonoscopy with sodium phosphates)
· rhabdomyolysis (breakdown of muscle tissue) – the resultant release of myoglobin in the blood affects the kidney; it can be caused by injury (especially crush injury and extensive blunt trauma), statins, stimulants and some other drugs
· hemolysis (breakdown of red blood cells) – the hemoglobin damages the tubules; it may be caused by various conditions such as sickle-cell disease, and lupus erythematosus
· multiple myeloma, either due to hypercalcemia or “cast nephropathy” (multiple myeloma can also cause chronic renal failure by a different mechanism)
· acute glomerulonephritis which may be due to a variety of causes, such as antiglomerular basement membrane disease/Goodpasture’s syndrome, Wegener’s granulomatosis or acute lupus nephritis with systemic lupus erythematosus
Post-renal (obstructive causes in the urinary tract) due to:
· medication interfering with normal bladder emptying (e.g. anticholinergics)
· kidney stones
· obstructed urinary catheter
Diagnosis
In general, renal failure is diagnosed when either creatinine or blood urea nitrogen tests are markedly elevated in an ill patient, especially when oliguria is present. Previous measurements of renal function may offer comparison, which is especially important if a patient is known to have chronic renal failure as well. If the cause is not apparent, a large amount of blood tests and examination of a urine specimen is typically performed to elucidate the cause of acute renal failure, medical ultrasonography of the renal tract is essential to rule out obstruction of the urinary tract.
Consensus criteria for the diagnosis of ARF are:
Risk: serum creatinine increased 1.5 times OR urine production of <0.5>
Injury: creatinine 2.0 times OR urine production <0.5>
Failure: creatinine 3.0 times OR creatinine >355 μmol/l (with a rise of >44) or urine output below 0.3 ml/kg for 24 h
Loss: persistent ARF or more than four weeks complete loss of kidney function.
Kidney biopsy may be performed in the setting of acute renal failure, to provide a definitive diagnosis and sometimes an idea of the prognosis, unless the cause is clear and appropriate screening investigations are reassuringly negative.
Kidney biopsy of the main case
(A) Kidney biopsy taken during renal failure and showing tubular casts (arrow), interstitial fibrosis, infiltration with lymphocytes and intact glomeruli. (B) A detailed image showing a tubular cast (solid arrow) with a ring of macrophages (dashed arrows).
Laboratory findings associated with acute renal failure
|
Clinical problem |
Mechanism |
Clinical considerations |
|
Nitrogenemia Elevated BUN levels |
Ongoing protein catabolism. Significantly decreased excretion |
Lower rate of production in neonates and persons with depleted protein stores. Increased in situations involving large amounts of necrotic tissue or extravasated blood. |
|
Elevated plasma creatinine levels |
Continued production. Significantly decreased excretion |
Production less affected by other factors. More sensitive measure of intensity of azotemia. Low in neonate because of small muscle mass relative to size |
|
Metabolic acidosis |
Continued endogenous acid production. Significantly decreased excretion. Depletion of extracellular and intracellular fluid buffers. |
Compensatory hyperventilation. Opisthotonos. Major threat to life. |
|
Hyponatremia |
Dilution of extracellular fluid. Decreased excretion of water. |
May develop cerebral signs. |
|
Hyperkalemia |
Ongoing protein catabolism. Decreased excretion compounded by metabolic acidosis. |
Most important electrolyte to be considered in acute renal failure. May contribute to cardiac arrhythmia. With ECG changes, major threat to life. Maybe lost from gastrointestinal tract. |
|
Hypocatcemia |
Associated with metabolic acidosis and hyperphosphatemia. |
During alkali therapy, may cause tetany. |
Treatment
Acute renal failure may be reversible if treated promptly and appropriately. Resuscitation must apply normotension and a normal cardiac output. The main interventions are monitoring fluid intake and output as closely as possible; insertion of a urinary catheter is useful for monitoring urine output as well as relieving possible bladder outlet obstruction, such as with an enlarged prostate. In the absence of fluid overload, administering intravenous fluids is typically the first step to improve renal function. Fluid administration may be monitored with the use of a central venous catheter to avoid over- or under-replacement of fluid. If the cause is obstruction of the urinary tract, relief of the obstruction (with a nephrostomy or urinary catheter) may be necessary. Metabolic acidosis and hyperkalemia, the two most serious biochemical manifestations of acute renal failure, may require medical treatment with sodium bicarbonate administration and antihyperkalemic measures, unless dialysis is required.
Should hypotension prove a persistent problem in the fluid replete patient, inotropes such as norepinephrine or dobutamine may be given to improve cardiac output and hence renal perfusion. While a useful pressor, there is no evidence to suggest that dopamine is of any specific benefit, and at least a suggestion of possible harm. A Swan-Ganz catheter may be used, to measure pulmonary artery occlusion pressure to provide a guide to left atrial pressure (and thus left heart function) as a target for inotropic support.
The use of diuretics such as furosemide, while widespread and sometimes convenient in ameliorating fluid overload, does not reduce the risk of complications and death. In practice, diuretics may simply mask things, making it more difficult to judge the adequacy of resuscitation.
Lack of improvement with fluid resuscitation, therapy-resistant hyperkalemia, metabolic acidosis, or fluid overload may necessitate artificial support in the form of dialysis or hemofiltration. Depending on the cause, a proportion of patients will never regain full renal function, thus having end stage renal failure requiring lifelong dialysis or a kidney transplant.
Dialysis
Chronic renal failure (CRF)
The kidneys are able to maintain the chemical composition of fluids withiormal limits until more than 50% of functional renal capacity is destroyed by disease or injury. Chronic renal insufficiency or failure begins when the diseased kidneys cao longer maintaiormal chemical structure of body fluids under normal conditions. Progressive deterioration over months or years produces a variety of clinical and biochemical disturbances that eventually culminate in the clinical syndrome known as uremia. The pattern of renal dysfunction is remarkably uniform no matter what disease process initiates the advanced disease. Renal vascular disorders such as hemolytic-uremic syndrome, vascular thrombosis, or cortical necrosis are less frequent causes.
Diagnostic criteria
I. Clinical:
· tiredness, fatigue, headache, loss of appetite, vomiting
· polyuria, nicturia, polydypsia, bone and joint pains, retardation of growth,
dryness and itching of skin
· muscular convulsions, paresthesias, signs of sensor or motor neuropathy,
· heart failure and hemodynamic disorders
II. Laboratory:
· decrease of glomerular filtration rate
· metabolic acidosis
· anemia
· decrease of thrombocytes’ adhesion
· hyperkalemia, hyperphosphatemia, hypocalcemia, hypoproteinemia, hyperuricemia
· isostenuria
· renal osteodystrophy
· X-ray examination of the chest may reveal cardiomegaly, hypertrophy of the left ventricle, aortectasia, lung’s edema, pleural exudates.
Causes of chronic renal failure
1. Glomerular diseases.
A) Glomerulonephritis:
ü of unknown etiology
ü associated with systemic lupus erythematosus (SLE), polyarteriitis
nodosa
ü Henoch-Schonlein vasculitis
B) Familial nephropathy:
– nephronophthisis
– Alport’s syndrome
C) Hemolytic uremic syndrome
D) Amyloidosis
E)Congenital anomalies:
ü bilateral renal dysplasia
ü congenital nephrotic syndrome
ü polycystic kidney
Clinical manifestations
The first evidence of difficulty is usually loss of normal energy and increased fatigue on exertion. For example, the child may prefer quiet, passive activities rather than participation in more active games and outdoor play. The child is usually somewhat pale, but it is often so inconspicuous that the change may not be evident to parents or others. Sometimes the blood pressure is elevated. As the disease progresses, other manifestations may appear. The child eats less well (especially breakfast), shows less interest iormal activities, such as schoolwork or play, and has an increased urinary output and a compensatory intake of fluid. For example, a previously dry child may wet the bed at night. Pallor becomes more evident as the skin develops a characteristic sallow, muddy appearance as the result of anemia and deposition of urochrome pigment in the skin. The child may complain of headache, muscle cramps, and nausea. Other signs and symptoms include weight loss, facial puffiness, malaise, bone or joint pain, growth retardation, dryness or itching of the skin, bruised skin, and sometimes sensory or motor loss. Amenorrhea is common in adolescent girls.
The therapy is generally instigated before the appearance of the uremic syndrome, although there are occasions in which the symptoms may be observed. Manifestations of untreated uremia reflect the progressive nature of the homeostatic disturbances and general toxicity. Gastrointestinal symptoms include anorexia and nausea and vomiting. Bleeding tendencies are apparent in bruises, bloody diarrheal stools, stomatitis, and bleeding from lips and mouth. There is intractable itching, probably related to hyperparathyroidism, and deposits of urea crystals appear on the skin as “uremic frost”. There may be an unpleasant “uremic” odor to the breath. Respirations become deeper as a result of metabolic acidosis, and circulatory overload is manifest by hypertension, congestive heart failure, and pulmonary edema. Neurologic involvement is reflected by progressive confusion, dulling of sensorium, and, ultimately, coma. Other signs may include tremors, muscular twitching, and seizures.
Therapy: carefull attention to nutrition, minimizing the exretory work of the kidneys, corticosteroids, immunosuppressive dmgs, non-steroid antiinflammatory dmgs, anticoagulation dmgs, antioxydants, peritoneal dialysis, hemodialysis, renal transplantation.
Diet
Dietary management is of paramount importance in children with chronic kidney disease. These patients have an altered metabolic milieu due to deranged kidney function. The challenge for pediatricians is to optimize the growth and development of children in this setting. The challenge for both pediatricians and dietitians is to make the diet interesting and palatable in order to ensure compliance. The goal is not only to add years to life but also to life to years.
Energy
Energy requirement should meet at least recommended dietary allowance (RDA) for normal children of same height age. If protein energy malnutrition (PEM) is present, it needs to be increased further to improve weight gain and linear growth. Calorie intake should be enough to enhance the efficiency of protein (protein-sparing effect) and to prevent the patient from lapsing into a catabolic state.
Poor intake is common in these patients due to anorexia, nausea and dietary restrictions. When use of chronological age does not account for the growth, height age should be the basis for energy estimation. Supplementation can be used as per requirement (enteral or parenteral nutrition as needed).
Protein
The diet should include 1.1-1.2 g/kg/d protein, with 60-70% protein from high biological value origin. Protein is required to maintain positive nitrogen balance for growth and maintain body protein turn over. The protein intake must be carefully controlled, avoiding protein malnutrition from an excessively restricted diet while avoiding toxicity from nitrogenous waste products from an excessively generous diet.
High biological value proteins are of utmost importance because they are beneficial in promoting muscle anabolism and decreasing muscle wasting.
Protein restriction is not recommended in children because it has not been shown to influence the decrease in renal function in children with chronic kidney disease.
Phosphorus and calcium
As the GFR progressively declines, excretion of phosphate decreases, and, hence, serum phosphorus levels increase. Because of this, care must be taken for the following:
Ø Dietary phosphorus restriction
Ø Regular phosphate binders with the meals
The elemental calcium intake recommended for pediatric patients with chronic kidney disease is as follows:
Ø Age 1-10 years: 500-600 mg/d
Ø Age 11-18 years: 800-1000 mg/d
High amounts of phosphorus affects growth in children and, if levels are high over a long period, may cause renal osteodystrophy. Prolonged elevation of serum calcium and phosphorus levels leads to vascular calcification. The daily elemental calcium requirement is about 80-100 mg/kg/d.
Potassium
The potassium requirement should be individualized depending on the serum potassium levels. Approximately 1600-2400 mg of potassium can be given.
Close watch should be kept on the potassium levels, and modifications can be made accordingly.
Hyperkalemia may occur due to excessive intake of high-potassium foods, catabolism, and other causes. Special attention should be given if the child is anuric. Leaching of pulses and vegetables should be suggested if the child is hyperkalemic. Daily bowel movements are important because the GI route accounts for as much as 30% of potassium excretion in patients with chronic renal failure.
Sodium and fluid
No added salt (NAS) and restriction of salty snacks is recommended.
If the child is hypertensive and edematous, further restriction of salt and fluid is emphasized. However, exceptions include diseases in which sodium is lost in the urine (salt-losing nephropathies). The allowance of salt depends on the presence of edema, hypertension, and administration of sodium-containing medications. Salt intake should be kept to less than 2400 mg/d.
Once these children progress to dialysis or opt for kidney transplantation, a dietician should be consulted again because the dietary requirements change.
Hemodialysis is a hemofiltration system that occurs outside the body. It requires an arteriovenous (AV) fistula or shunt to be placed in a large vessel. This central line provides access to the blood system to pump the blood out from the body to an external extracorporeal circuit and through a filtration system. This serves to remove the body’s waste products that cao longer be effectively filtered through the kidneys. This arteriovenous shunt in a large vessel requires surgical placement. The nurse must aseptically maintain it. Hemodialysis can be performed on an intermittent time-cycled basis, either in a hospital, dialysis center, or home setting. It is usually a 3 to 4 hour procedure repeated 3 to 4 times per week. It is more efficient at removing nitrogenous wastes than any other form of dialysis.
Hemodialysis
Peritoneal dialysis requires the placement of a catheter into the peritoneal cavity for the purposes of removing excess fluids, solutes, and nitrogenous wastes (Figure 22-10). This placement may or may not require an open surgical procedure. It usually does not require a heparinized line. The treatment or filtration process involves the slow flow of fluid through the catheter into the peritoneal cavity until the desired fluid level has been administered. At that time a clamp is put in place allowing the fluid to dwell for a time in the peritoneal cavity to remove waste products. When the clamp is released, the fluid drains into the dialysis system. This cycle is repeated either automatically or manually four to five times per day. The procedure is usually repeated for several days and is normally done at home. Peritoneal dialysis is problematic for infants requiring dialysis, as the clearance of toxic wastes, solutes, and fluids is slow. Their abdominal areas are small and, if the treatment is not successful, the hypervolemia may be worse, a conditioot tolerated well by small infants.
Peritoneal dialysis
Hemofiltration is a continuous form of dialysis by means of a continuous arteriovenous (CAV) or venovenous (CW) shunt. These shunts, like hemodialysis, require an extracorporeal circuit through which the blood flows into a filter system. The filter is placed between the arterial and venous lines along with a collecting bag. The blood flows from the child through the circuit continuously to remove nitrogenous wastes, solutes, and fluid. When the arteriovenous shunt is used, movement of the fluid is caused by the body’s own pressure gradient (hydrostatic pressure from cardiac output and oncotic pressure from plasma proteins) rather than an external pumping device. If the venovenous shunt is used, a pump is necessary to move the blood through two separate venous cannulas or two ports in mul-tilumen cannula (Madder & Milberger, 1996). Both ports are in veins so blood leaves through a venous route and returns via a vein. Either of these ultrafiltration systems has the advantage of using a very slow process that continuously adjusts as the body’s solute load changes. The pres– sure of the body’s own plasma proteins helps regulate the system so there is less stress on it. The circuit is heparinized so there is a danger of bleeding with this type of dialysis. However, this danger is less than with hemodialysis because less volume of blood flows through the circuit.
Treatment for the child with chronic renal failure and ESRF is aimed at restoring or maintaining fluid and electrolyte balance. If edema is present, then fluid restriction and sodium and potassium restriction may be necessary. Diuretics are used if edema is significant. Antihypertensive medications are given if hypertension is present. Protein intake may be restricted because of the kidney’s inability to rid the body of waste products. Phosphorus is restricted in order to increase the calcium levels. If calcium levels are maintained, then there is less chance of bone disease that can result when calcium levels are low. Vitamin D supplementation may be given. The result is that vitamin D will be present to boost the calcium levels to prevent bone disease. Aluminum hydroxy gel may be given to bind with phosphorus and decrease the gastrointestinal absorption. This medication should only be used on a short-term basis as aluminum levels can become high and result in seizures. Calcium carbonate will achieve the same result and is not toxic even to infants.
Experimental therapies include erythropoietin to combat anemia and growth hormone to boost linear growth. Immunosuppressive therapy is also used especially if the child is going to require renal transplantation. While this immuno–suppressive therapy is not experimental, the combination of medications (more than one immunosuppressive medication at a time) is undergoing research. For those children with ESRF, dialysis and/or renal transplantation are the only treatment options.
Renal transplantation is usually reserved for children for whom medication and dietary management of fluid and electrolyte balance and hypertension have been unsuccessful. These children have ESRF. They may or may not have been maintained on dialysis for a long period of time prior to the transplant. Transplants can be performed on infants. The surgical team and the family make the determination of the candidate for a transplant. In some institutions an ethics committee also looks at quality of life issues to help in the decision-making process. The question they usually ask is “What will the long-term quality of life be for this child if the transplant is done?” Unfortunately there are no guarantees with this type of surgery. The usual candidates for transplants are those who can withstand a surgical intervention, are in good nutritional status, and are not severely immuno–compromised.
Kidneys for transplantation are obtained either through living donors—usually close relatives—or cadavers. Tissue typing to determine a match requires meticulous tests similar to crossmatching for blood transfusions. Close relatives are most likely to be a very good tissue match, but even then there is a chance of graft (the transplanted kidney) or organ rejection. Cyclosporine, azathioprine (Imuran) and prednisone or prednisolone are used to suppress the natural immune response. Organ rejection is known as graft versus host disease, which occurs when the transplanted organ fights against its host, creating an exaggerated immune response to rid the body of the foreign organ. This reaction can be life-threatening. Most renal transplants are not lost by rejection but the tissue dies from vascular thrombus or clots in the renal vessels.
Transplantation is just one aspect of ESRF treatment. Post-transplantation, immunosuppressive medications are required for life. Dietary restrictions may still be necessary especially regarding protein intake. Medications for hypertension and diuretics may still be needed following surgery.
Uremic coma
Uremic coma develops at the chronic kidney diseases with severe functional insufficiency. A coma develops slowly with proof head ache and vomit, common trouble, insomnia.
Gradually a child becomes indifferent, sleepy, soporosis and eventually falls in a deep coma. In the last phase a child lies with expression of indifference, pale, with the easy edema of eyelids and narrowed pupils. A skin is dry, swollen. Breathing is deep, often to the type Chayne–Stokes or Kussmaul. Cardiac activity is broken. There are high cardiac shove, increased П tone above an aorta, promotion of AP. Friction of pericardium. In vomit there are masses admixture of blood . Toxic diarrhea is present. There is the white disk of visual nerve on an eyeing botton. Tendon reflexes are promoted. Convulsions appear in the final stage of disease. In a blood: anaemia, nitrogenemia, increase of urinary acid and creatinini, decline of alkaline reserve. In urine: decline of specific gravity, cylinduria, erythrocyturia, proteinuria.
Sopor
Masses admixture of blood in vomiting
A coma at eclampsic uremia (pseudouremia, chloremia) can occur very acutely, suddenly to the exposure of signs of acute glomerulonephritis. More frequently begins from generelized tonico-clonic convultions and at once is deep. In most cases develops at presence of signs of acute diffuse glomerulonephfitis, to which precede great head ache, vomit, disorders of sight and ear. Quite often there are the additional focal symptoms related to the spasm of cerebral vessels: pathological reflexes, hemianopsia, aphasia, temporal paresises, fibril convultions of muscles and other
During the attack of convultions the breathing is stridorous, breathing normalization comes after an attack. Tones of heart are loud, high cardiac shove, the accent of II tone on an aorta, increase of АP. Skin is pale, edenematous, pupils are narrow, stagnant, edenematous nipples and spasm of vessels on an eyeing botton. In a blood: hyperelectrolitemia with hyperchloremia and hyperkaliemia, hypocalciemia. In urine: oliguria, haematuria, proteinuria, cylindrurtia.
|
Signs |
Coma uremia |
Coma pseudouremica (eclampsic) |
|
Previous or basic disease |
Chronic nephrite |
Acute nephrite |
|
Beginning |
Slow with progress |
Sudden, acute with convultions |
|
Motive activity |
Mioclonic convultions in different areas of body, pathological grabbing reflex |
Increase of muscular excitability, strengthening of tendon reflexes, temporal mono – or hemiparesis, mono or hemiplegia (and temporal convultions) |
|
Convultions |
– |
+++ |
|
Breathing |
Deep, toxic, sometimes Cheyne-Stokes, smell of ammonia (urines) |
Noisy, strydorosis |
|
Сardio-vascular changes |
Accent of ІІ tone on an aorta, increase of АP, noise, friction of pericardium |
Bradycardia, increase of АP |
|
Change of digestion |
Vomit, sometimes diarrhea |
Vomit |
|
Liver |
Often enlarged |
Often enlarged |
|
Eyes |
Pupils are narrowed, decline of acuteness of sight |
Edematous nipples |
|
Skin |
Dry, severe itch, tracks of scratch, edematous |
Pale |
|
Edemata |
Small |
Expressly severe |
|
Blood |
Acidosis, nitrogenemia, hyperkaliemia, hypocalciemia |
Hypochloremia, insignificant nitrogenemia |
|
Urine |
Poliuria, low specific gravity, diminishment of amount of albumini and cystic elements |
Albuminuria, hematuria, cylindruria, high specific gravity |
The hypochloremia coma develops at unrestrained vomit: poisonings, toxicoinfections, acute gastro-intestinal disorders, surgical diseases of digestive channel (impassability, invagination), afteroperative vomit, protracted acetonemic vomit, massive and protracted sweatness, reception of saldiuretics.
It develops slowly. A child becomes adynamic with hyperreflexia. Quite often there is tetania, catalepsy, fibril convulsions. Sharp lines of face, eyeballs are soft, a skin is dry, turgor is reduced. Breathing is superficial and increased. Tachycardia, arterial blood pressure is low. Blood: high hematocriti, hypernitrogenemia, hypochloremia, hypokaliemia. In urine: small proteinuria and erythrocyturia.
Help on a prehospital stage at uremic coma
1. At sopor to wash a stomach and intestine by 2-3 % sodium solution hydrocarbonati (washing of stomach in the comatose state is conducted only after intubation).
2. To limit the receipt in the organism of salt, proteins.
3. With the purpose of the detoxication intravenously in drops introduction of 5 % Glucose solution 10-20 ml/kg of mass with 2-3 ml 5 % solution of ascorbic acid.
4. At severe vomit and diarrhea to reduce hypochloremia intravenously in drops introduction 5 % of Glucose solution in half with isotonic solution of sodium chloride .
5. At vomit: Motillium – 1/2-1 tablets 2 times per day, Bromopridi 1 candle (10 mg) 1-2 times for a day, Cerucali – 0,05 mg/kg the masses ( for one occasion dose) intramuscular, Clemastini – 0,5-1 mg ( for one occasion dose) intramuscular to children of 6-12 years old .
6. At convulsions: Seduxeni 0,5 % solution intramuscular or intravenously streamly in one occasion dose 0,1 ml/kg the masses, but not more than 2-3 ml; 20 % solution of Oxybutirati sodium 70-100 mg/kg of mass intravenously streamly slowly on 20 ml isotonic solution of chloride sodium or 5 % Glucose solution.
7. Oxygen therapy by clean moistened oxygen.
8. Hospitalization in the intensive unit or chamber of intensive therapy.
Help on a hospital stage
1. Intravenously in drops 5 % Glucose solution , isotonic solution of sodium chloride or Ringer solution in even proportions in the total dose of 15 ml/kg of mass + volume which equals day’s diuresis + amount of the liquid lost with vomit and diarrhea, on every degree of the promoted temperature of body ad 5 ml on every kilogram of mass.
2. At oliguria intravenously in drops 15 % Mannitoli solution 0,5-1 g/kg of masses per day, dividing into 2-3 introductions. Parallel is appointed 1 % solution of Lazix intravenously streamly in one occasion dose 1-2 mg/kg of mass, 2,4 % Euphyllini solution in one occasion dose 2-3 mg/kg of mass intravenously streamly.
3. For liquidation of acydosis intravenously in drops very slowly 4 % solution of sodium hydrocarbonati 4 ml/kg of mass, to enter by drops doses under the control ABB.
4. At hyperkaliemia 10 % Glucose solution intravenously in drops from a calculation 0,5 g/kg of mass with insulin (1U of insulin for a 4-
5. At acute cardiac insufficiency intravenously in drops Dophamini from the calculation of a 3-5 mkg/kg of mass in 1 minute (4 % to divorce solution of Dophamini in 400 ml 5 % Glucose solution , in 1 ml will be 500 mkg Dophamini).
6. At severe anaemia transfusion of red corpuscles mass 5 ml/kg of mass of body.
7. At convultions: 0,5 % solution of Seduxeni intramuscular or intravenously streamly in one occasion dose 0,1 ml/kg of mass, but not more than 2-3 ml, or 20 % solution of Oxybutirati sodium 70-100 mg/kg of mass intravenously streamly slowly on 20 ml isotonic solution of sodium chloride or 5 % Glucose solution .
8. Oxygen therapy by 40 % moistened warmed-up to 22-24 0С oxygen through a nasal catheter.
9. Lespenephrili 20-30 drops 8-10 times per.
10. Washing of stomach (if in a coma, after intubation) and intestine by 2-3 % of solution of sodium hydrocarbonati; enterosorbents: absorbent carbon 1 g/kg of mass, Enterodesi 2-
11. At absence of effect – hemodialisis, which the indications are the increasing the blood urea to 20-33 mmol/l, creatinini – to 0,64-1,2 mmol/l, potassium – to 6-6,5 mmol/l, decline of alkaline reserve below 12 mmol/l, during glumerules filtration below 5 ml/mn.
Hemodialisis
Prognosis
Acute renal failure in children is very serious complication, especially in the first two days of life. Prevention is the early diagnosis of congenital and hereditary kidney diseases. Such children should be protected from various stress conditions. They are contraindicated vaccinations. It is necessary active treatment of infectious diseases.
Referens:
A – Basic:
1. Pediatrics. Textbook. / O. V. Tiazhka, T. V. Pochinok, A. N. Antoshkina et al. / edited by O. Tiazhka – Vinnytsia : Nova Knyha Publishers, 2011 – 584 pp. : il.
2. ISBN 978-966-382-355-3Nelson Textbook of Pediatrics, 19th Edition Kliegman, Behrman. Published by Jenson & Stanton, 2011, 2608. ISBN: 978-080-892-420-3.
3. Illustrated Textbook of Paediatrics, 4th Edition. Published by Lissauer & Clayden, 2012, 552 p. ISBN: 978-072-343-566-2.
4. Denial Bernstein. Pediatrics for medical Students. – Second edition, 2012. – 650 p.
2. http://www.merckmanuals.com/professional/index.html
