Lesson N 10.
Clinical discussion. Glomerulonephritis: etiology, pathogenesis, classification, clinical pattern. Complications, treatment. Participation of a doctor-dentist in the prophylaxis of glomerulonephritis.
Clinical discussion. Pyelonephritis: etiology, pathogenesis, classification, clinical pattern. Diagnostics, treatment. Participoation of a doctor-dentist in the prophylaxis of pyelonephritis.
Clinical discussion. Kidney amyloidosis. Renal failure. Uremia. Clinical pattern, treatment. Participoation of a doctor-dentist in the prophylaxis.
Structure of the nephrone
Diffuse glomerulonephritis is the general infectious allergic disease with predominant affection of the glomerular vessels. Acute and chronic glomerulonephritis are distinguished.
Aetiology. Acute diffuse glomerulonephritis usually develop after acute infectious diseases, such as tonsillitis, scarlet fever, acute respiratory diseases, pneumonia, and otitis. Especially important are disease caused by group A haemolytic streptococcus, most frequently of type XII. But nephritis can arise also after infectious diseases caused by other bacteria e.g. pneumococci or staphylococci. Acute nephritis sometimes develops following overcooling, especially in damp weather. Cases were reported acute nephritis developing after vaccination.
Pathogenesis. Acute nephritis typically arises not during an infectious disease but only following a period of time, usually 2-3 weeks later. Attempts to isolate the streptococcus from the kidney tissue end in failure. Thus, the onset of acute nephritis usually coincides with the period antibodies to streptococcus are produced. This indicates that acute nephritis is not simply an infectious disease but an infectious al disease.
It is suggested that bacterial antigens, that get into the blood during infection, injure the kidney tissue, whose affected proteins art as an antigen to stimulate the production of the corresponding antibodies in the reticuloendothelial system. The antigen-antibody complexes are fixed in the endothelial and epithelial cells of the renal glomeruli and also in the basal membrane of the glomerular capillaries to cause their injury. Both kidneys are always involved in acute diffuse glomerulonephritis and all glomeruli are equally affected. This distinguishes the affection from focal nephritis and confirms its allergic nature.
It is necessary to note that both the glomerular capillaries and vessels of the other organs and tissues are affected in acute glomerulonephritis. Nephritis is thus the general vascular disease. Cases have been described when in the presence of a marked clinical picture of the disease (oedema, hypertension), the urinary symptoms were insignificant or absent. But as a rule the glomerular apparatus of the kidneys is affected in acute nephritis which is explained by the specific character of their function as the excretory organ.
Clinical picture. The clinical picture of acute glomerulonephritis is quite specific and is determined by the main three syndromes: oedema, arterial hypertension, and changes in the urine (haematuria and proteinuria). The patients would usually complain of oedema, which arise first on the face, under the eyes, and then extend onto the entire body and the extremities. Development of oedema is explained by disordered capillary permeability and aldosterone hypersecretion by the adrenal cortex. Headache and heaviness in the head are frequent symptoms. They are explained by increased arterial pressure and, in some cases, intracranial pressure. Vision can be deranged due to spasm of the retinal vessels and haemorrhages into the retina. Many patients complain of general fatigue and reduced work capacity.
In the presence of a pronounced oedema and massive pleural effusion, and when the heart muscle is overloaded due to markedly increased arterial pressure, patients with acute nephritis suffer from severe dyspnoea, sometimes with attacks of asphyxia (like in cardiac asthma).
Edema
The patient with acute nephritis would often complain of dull lumbar pain. The gravity of the disease depends on the degree of oliguria. The diuresis decreases while the patient may have frequent tenesmus. Complete anuria occurs in some cases. If haematuria is marked, the urine looks like meat wastes.
Inspection of the patient reveals his specific appearance: pallid skin, edematous face, swollen eyelids, and oedema of the trunk. Some patients assume the forced semireclining or sitting position because of pronounced dyspnoea. Renal eclampsia occurs in grave cases. The onset of an eclampsia attack is heralded by increasing arterial pressure and a severe headache. The extent and the character of oedema can be established by palpation. The pulse of the patient should also be felt. Acute nephritis is characterized by a tense pulse which is sometimes slow. The apex beat is somewhat shifted to the left and increased due to myocardial hypertrophy which soon develops in the presence of arterial hypertension.
Percussion of the chest in the presence of generalized oedema reveals free fluid in the pleural cavity (transudate) and congestion in the lung root region (dulled tympany). The left border of the heart extends beyond the corresponding midclavicular line.
Normal or harsh respiration is heard by auscultation. In the presence of pronounced congestion, dry and moist congestive rales are heard.
Auscultation of the heart reveals bradycardia (due to the reflex transmitted in increased pressure from the aorta onto the vagus nerve through n. depressor).
The first sound is sometimes decreased at the apex. If the heart muske is much overloaded, the gallop rhythm is heard. The second sound isd usually accentuated over the aorta due to increased arterial pressure.
X-ray studies of the chest confirm the presence of pleural effusion and congestion in the lung roots. Dilatation and hypertrophy of the left ventricle are clearly determined (the heart apex is rounded). Sphygmomanometry is of great help in establishing a diagnosis. It reveals one of the main symptoms of acute nephritis, i.e. arterial hypertension. Systolic pressure increases to 200—220 mm Hg, but in some cases it is not so high. Diastolic pressure increases to 100-160 mm Hg almost in all cases.
Electrocardiography reveals signs of hypertrophy and overload of the left-ventricular myocardium. The amplitude of ECG waves decreases in pronounced oedema of the trunk.
Kidney at ultrasound examination
Changes in the urine are characteristic of acute nephritis. During development of oedema, diuresis usually decreases to oliguria. The urine of patients with acute nephritis usually contains much protein and erythrocytes due to the increased permeability of the renal capillaries. If haematuria is pronounced, urine can be reddish-brown (the colour of meat wastes). Microscopy of the urinary sediment usually reveals the presence of casts (mainly hyaline casts) and cells of renal epithelium. The nitrogen excretory function of the kidneys is usually not affected in acute nephritis. Nitrogenous slags can only accumulate in the blood in serious cases attended by anuria. The clearance tests reveal more or less considerable reduction of glomerular filtration.
The infectious allergic character of acute glomerulonephritis is confirmed by immunological shifts: the content of a2– and b-globulins in the blood increases during the acute period.
Active leucocytes in urine
Acute glomerulonephritis often proceeds without pronounced symptoms which make it difficult to identify it and hence to prescribe the appropriate treatment. But mild and indistinct forms of glomerulonephritis, like acute forms of this disease with classical clinical symptoms, give rise to chronic glomerulonephritis, unless the appropriate therapy is given.
Renal scanogram in a healthy individual (1) and pyelonephritis (2)
Contrast X-ray examination of kidneys
Plaine X-ray, contrast excretory urogram, radionucleic examination of kidneys
Renal eclampsia. The gravest and even dramatic complication of acute glomerulonephritis is renal eclampsia which occurs in 4-10 per cent of patients (mostly in children and women). During a convulsive attack, the patient may be heavily contused or his ribs may be fractured. Cases reported where patients died from cerebral circulatory disorders or oedema; true, such cases are rare. Attacks of eclampsia usually leave no consequence. It is interesting to note that eclampsia sometimes serves, .is a stimulus to a rapid regress of the disease and patient’s recovery.
Degree of nephroptosis (I, II, III)
Selective transfemoralnal angiogram. The right renal artery shows nephroptosis
Course. Acute glomerulonephritis usually lasts only a few weeks or months. The first sign of beginning recovery is resolution of oedema and further decrease in arterial pressure. Small haematuria and proteinuria can persist for months following disappearance of the main symptoms. Some patients do not recover completely and the disease becomes chronic.
Treatment. Patients with acute nephritis should be taken to hospital. It is important that the air in the ward should be warm and dry; drafts should be absent. Sodium chloride intake should be restricted to 0.5-1.5 g a day, which promotes resolution of oedema and normalization of arterial pressure. Protein intake should also be slightly decreased (at the expense of meat protein).
Prednisolone and other corticosteroid hormones having anti-allergic and anti-inflammatory properties are efficacious means of pathogenetic therapy of acute nephritis. Hypotensive preparations are given to control hypertension; furocemid and other diuretics should be given to remove oedema.
Prophylaxis. Hardening of the body and also thorough sanation of the infection foci (carious teeth, chronic tonsillitis, sinusitis, and the like) are required.
CHRONIC GLOMERULONEPHRITIS
Aetiology and pathogenesis. Chronic diffuse glomerulonephritis is a relatively common disease. It is often secondary to the acute form of this disease if the patient is not timely and properly treated. In other patients, chronic glomerulonephritis occurs suddenly, without acute nephritis in their anamnesis, but it can be suspected that the chronic disease was preceded by acute nephritis which however was latent, without manifest symptoms, and therefore not identified in proper time.
Chronic diffuse glomerulonephritis can sometimes be secondary to nephropathy of pregnancy which was not treated properly.
Great importance is now attached to the auto-immune mechanism in the pathogenesis of chronic glomerulonephritis. Antibodies to altered proteins of the renal tissue are probably formed in patients with the disease, in addition to formation of antibodies to streptococcus. This maintains the inflammatory process in the kidneys and is the cause of chronic progressive course of the disease.
Pathological anatomy. The kidneys are not enlarged, or enlarged only slightly during the first period of the disease, which lasts several years. In the final stage of the disease, the kidneys are markedly diminished in size, their surface is granular, the renal tissue is firm (arteriosclerotic kidney). Microscopy in chronic nephritis reveals mostly intracapillary inflammation in the glomeruli with gradual obliteration of the capillary loops and the capsule cavity and conversion of the glomerulus into a scar or hyaline node. Dystrophic changes occur in the epithelium of the renal tubules.
Clinical picture. Two periods can be easily distinguished in the of the disease: the first period, when the nitrogen secretory function of the kidneys is impaired only insignificantly (the stage of renal compensation), and the second period, during which this function is affected substantially (the stage of renal decompensation).
The symptoms of the first period are the same as in acute nephritis. The patient may complain of weakness, more or less persistent headache, dizziness, and oedema. But the gravity of these symptoms is usually less significant than in acute nephritis. The disease is often asymptomatic and is only revealed accidentally, during out-patient examination. Objective studies help to establish increased arterial pressure and hypertrophy of the left ventricle. Urinalysis reveals proteinuria and cylindruria. The presence of waxy casts is especially important diagnostically. The urinary sediment usually contains a small quantity (less frequently, considerable quantity) of leached erythrocytes. The blood serum cholesterol content is increased. More or less significant hypoproteinaemia is observed due to permanent teinuria.
Symptoms of the second, or final, period of the disease gradually due to the progressive nephrosclerosis. Low indices of clearance tests indicate decreased quantity of functioning kidney tissue. The filtration capacity of the kidneys remains unchanged for a long time and only decreases during exacerbation of the process. The concentration capacity of the kidneys gradually decreases along with the decrease in the specific gravity of the urine. Removal oitrogenous slags from the body is maintained during this period by polyuria (evacuation of much liquid from the body). Nocturnal diuresis increases by the compensatory mechanism as well: it is two thirds-one half of the daily diuresis (nycturia). As the concentration capacity of the kidneys is affected to a greater extent, the specific gravity of the urine becomes low and its variations between 1.009 and 1.011 during the course of the day (and under the effect of dry food) are insignificant (isohyposthenuria). The content of nitrogenous slags in the blood of patients (urea, creatinine, indican) increases during this period.
Symptoms of uraemia develop: weakness becomes more considerable, the patient complains of lassitude, headache, nausea, skin itching, unpleasant ammonium breath, and impaired vision. Not long before death, the patients develop uraemic coma.
Facies nephritica
Course. Chronic nephritis usually lasts from 2-3 to 10-15 years. The first period of the disease (renal compensation) is long; the second period (decompensation) is shorter. During the course of the disease, there occur more or less prolonged periods of exacerbation, which are usually provoked by cooling or infections; exacerbations are followed by remissions.
Several clinical forms of chronic glomerulonephritis are differentiated by the character of its course and prevailing symptoms. The nephrotic form is characterized by oedema, the urinary syndrome, and a comparatively rapid course. The hypertensive form is comparatively benign and is characterized by the hypertensive syndrome and insignificant changes in the urine. The mixed form is characterized by oedema, changes in the urine, and arterial hypertension. This form of glomerulonephritis is the gravest and comparatively rapid: a pronounced renal failure develops in 2-3 years. Finally, there is the latent form of the disease, which is not manifested by oedema or pronounced hypertension; the changes in the urine are only insignificant; renal failure develops at late terms, often only in 10- 15 years. As a rule, the patient dies of renal failure.
Treatment. Patients with exacerbations are prescribed bed-rest, a dairy and vegetable diet with restricted sodium chloride (to 1.5-2.5 g/day) and containing at least 1 g/kg protein. The daily protein intake in the nephrotic form and hypoproteinaemia should be slightly increased. Foci of chronic infection (carious teeth, tonsillitis, etc.) should be treated. Infectious foci are treated with antibiotics. Good effect in the treatment of exacerbated nephritis (nephritic form of diffuse glomerulonephritis) is attained with prolonged use of chloroquine diphosphate (in the absence of marked hypertension or azotaemia). The course of treatment continues for several months. Stable clinical remission and even recovery of patients can sometimes be obtained with this therapy.
Symptomatic therapy in hypertensive and oedematous forms of chronic nephritis includes hypotonics and diuretics (hypothiazide, furocemid). Sanatorium therapy is often very helpful to patients with hypertensive and nephrotic forms of glomerulonephritis with compensated renal function.
Control of azotaemia is important in the treatment of uraemia. The intake of animal protein (meat) should be limited to 18-30 g/day. Broad spectrum antibiotics and also sour milk products (yoghourt, soar milk) are given to inhibit the putrefactive process in the intestine. In the absence of tendency to oedema, ample liquid is indicated. Group B vitamins, ascorbic acid, glucose, repeated blood transfusions, gastric lavage with sodium hydrocarbonate, sodium hydrocarbonate enema are used to control toxicosis. Peritoneal dialysis and haemodialysis (artificial kidney) are more effective means to control uraemic toxicosis. These means do not remove the cause,of uraemia but only prolong the patient’s life. More prospective treatment of severe forms of chronic nephritis is transplantation of the kidneys.
Hemodialisis
Prophylaxis. Prophylaxis consists in timely treatment of acute and chronic focal infections (tonsillitis, sinusitis, carious teeth, paradontosis, etc.). Patients with chronic glomerulonephritis should he regularly inspected.
Pyelonephritis
Pyelonephritis is a serious bacterial infection of the kidney that can be acute or chronic.
Description of Pyelonephritis
One of the most common renal diseases, acute pyelonephritis is a sudden inflammation caused by bacteria. It primarily affects the interstitial area and the renal pelvis or, less often, the renal tubules.
Chronic pyelonephritis is persistent kidney inflammation that can scar the kidneys and may lead to chronic renal failure. This disease is most common in patients who are predisposed to recurrent acute pyelonephritis, such as those with urinary obstructions or vesicoureteral reflux.
Causes and Risk Factors of Pyelonephritis
Doctors believe that the bacterial infection causing pyelonephritis may sometimes develop elsewhere in the body and travel through the bloodstream to the kidney. Far more commonly, however, the infection is the result of bacteria from outside the body traveling back up the urinary stream through the urethra to the bladder and eventually to the kidneys, in which case it is known as an ascending infection. This may explain why women, whose urethras are short and in close proximity to the anus, a potential source of bacteria, have four times as many cases of pyelonephritis as men.
The flow of urine backward is known as reflux and may be caused by an anatomical defect or by an obstruction. In the former case, instead of a tight valve between the bladder and the ureter, there is a wide opening. When the bladder contracts during urination, the urine goes both ways, out through the urethra and back up through the ureters. The defect is not easy to correct and those who have it are subject to repeat infections.
Obstructions that cause reflux in women are commonly in the form of a stricture, or scar tissue, itself formed from infection or inflammation in the urethra. In young men, such strictures form less often and usually are a consequence of a sexually transmitted infection. In older men, the prostate is commonly responsible for obstruction to the flow of urine.
Reflux can also be caused by the insertion of catheters or instruments such as cystoscopes for diagnosis or treatment. The introduction of any foreign body into an area of obstruction is fraught with danger of infection which can be more difficult to treat.
Symptoms of Pyelonephritis
No matter what the underlying cause, the symptoms of acute bacterial pyelonephritis are often the same. The first indications are usually shaking chills, accompanied by a high fever and pain in the joints and muscles including flank pain. Attention may not be drawn to the kidneys at all.
The situation may be especially confusing in children, when high temperature may suddenly bring on a seizure or a change in mental state, or in the aged, where fever may bring confusion, or the infection may be masked by generalized aches and pains.
There may be irritative voiding symptoms (burning when urinating, a sense of urgency, or increased frequency of urination).
In acute infections, the symptoms develop rapidly, the fever noted first, followed by possible changes in the color of the urine, and then tenderness in the flank. As the kidney becomes more inflamed, pain, loss of appetite, headache, and all the general effects of infection develop. This type of kidney pain differs from renal colic pain of kidney stones in that it is continuous and does not come in waves, stays in one spot, and may be worse by moving around.
While patients with chronic pyelonephritis may have acute infections, sometimes there are no symptoms, or the symptoms may be so mild that they go unnoticed. This carries the risk that the infectious inflammatory disease may progress slowly undetected over many years until there is enough deterioration to produce kidney failure. Thus, hypertension (high blood pressure) or anemia or symptoms related to renal insufficiency may be the first indication of trouble. Unfortunately, irreversible damage may have already taken place.
Diagnosis of Pyelonephritis
Your physician will take a medical history, perform a physical exam, and recommend tests including blood tests and blood cultures, urinalysis and urine culture, and possibly an ultrasound study of the kidneys.
Treatment of Pyelonephritis
Treatment centers on antibiotic therapy appropriate to the specific infecting organism, after identification by urine culture. When the infecting organism cannot be identified, therapy usually consists of a broad-spectrum antibiotic. Symptoms may disappear after several days of antibiotic therapy. Although urine usually becomes sterile within 48 to 72 hours, the course of such therapy is 21 days.
Patients with severe infections or complicating factors require hospitalization at least initially. In some patients, surgery may be necessary to relieve obstruction or correct an anatomical anomaly.
Follow-up treatment includes reculturing the urine several weeks after drug therapy stops in order to rule-out reinfection.
Patients at high risk of recurring urinary tract and kidney infections – such as those with prolonged use of an indwelling (Foley) catheter- require long-term follow-up.
