Special Pathology. Diseases of the urinary system come among the first in the list of diseases the most frequently occurring

Diseases of the urinary system come among the first in the list of diseases the most frequently occurring. In some cases the kidneys may be the locus of primary pathology. These are comparatively rare congenital abnormalities and genetic nephropathies. Inflammatory affections of the renal parenchyma, such as diffuse glomerulonephritis of infectious allergic nature, pyelonephritis arising in inflammatory processes of the urinary tract (cystitis, pyelitis) due to extension of inflammation onto the renal parenchyma, and focal nephritis in sepsis occur more commonly. The group of metabolic-dystrophic diseases of the kidneys includes their acute affections in various poisonings with nephrotoxic substances, in shock, and also chronic diseases such as amyloidosis and, to a certain extent, nephrolithiasis. The kidneys are often the site of tumours (especially fre­quently hypernephroid cancer or hypernephroma). Affections of the renal vessels are not infrequent. Traumatic affections of the kidneys often occur in surgery and treatment of urinary diseases.

The other group includes affections of the kidneys that are secondary to diseases of the other organs and systems: essential hypertension, atherosclerosis, diabetes mellitus, gout, collagenosis, general infections, etc.

In many untreated or improperly treated cases, primary or secondary affections of the kidneys cause dystrophic changes in nephrons, develop­ment of connective tissue with its subsequent cicatrization and cirrhosis of the kidneys (nephrosclerosis) which is manifested clinically by signs of pro­gressive renal failure (see " Renal Failure").

Diffuse Glomerulonephritis

Diffuse glomerulonephritis is the general infectious allergic disease with predominant affection of the glomerular vessels. Acute and chronic glomerulonephritis are distinguished.

I

ACUTE GLOMERULONEPHRITIS

Aetiology. Acute diffuse glomerulonephritis usualy develops after acute infectious diseases, such as tonsillitis, scarlet fever, acute respiratory diseases, pneumonia, and otitis. Especially important are diseases 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 of 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 when antibodies to streptococcus are produced. This indicates that acute nephritis is not simply an infectious disease but an infectious allergic disease.

It is suggested that bacterial antigens, that get into the blood during in­fection, injure the kidney tissue, whose affected proteins act 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.

Pathological anatomy. The kidneys of those who died from acute nephritis are of normal size or slightly enlarged; their colour is brown or greyish-brown. Malpighi corpuscles, in the form of small tubercles, can be seen on section. Microscopy of the renal tissue in the initial stage of the disease reveals enlarged and hyperaemic glomeruli; during further progress of the disease, microscopy reveals ischaemia of the glomeruli due to spasm of the capillary loops, fibrinoid swelling of the capillary walls, proliferation of their endothelium, accumulation of coagulated proteinous exudate in the space between the capillary loops and the glomerular capsule, blood stasis, thrombosis of the capillary loops, and haemorrhages. Pathological changes occur in both kidneys in all cases. Epithelium of the renal tubules is affected less

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markedly. Intra- and extracapillary glomerulonephritis is mostly differentiated; depending o
the character of the inflammation, glomerulonephritis may be exudative (serous, fibrinou
and haemorrhagic) and productive. '

At later stages of the disease, inflammatory phenomena subside in renal tissue, prolifera­tion of endothelium in glomerular loops decreases, and patency of the capillaries is restored

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 pro-teinuria). 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).

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, oedematous 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 heart apex. If the heart muscle is much overloaded, the gallop rhythm is heard. The second sound is 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). Sphygmomanome-try 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.

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 7-globulins in the blood increases during the acute period.

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.

The gravest and even dramatic (Tareev) 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 were reported where patients died from cerebral circulatory disorders or lung oedema; true, such cases are rare. Attacks of eclampsia usually leave no consequence. It is interesting to note that eclampsia sometimes serves as a stimulus to a rapid regress of the disease and patient's recovery.

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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. Rauvolfia is 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. Chronic nephritis is one of the three classical forms of Bright's disease.

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 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 a hyaline node. Dystrophic changes occur in the epithelium of the renal tubules.

Clinical picture. Two periods can be easily distinguished in the course 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, ver­tigo, 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 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 Oess frequently, considerable quantity) of leach­ed erythrocytes. The blood serum cholesterol content is increased. More or less significant hypoproteinaemia is observed due to permanent pro­teinuria.

Symptoms of the second, or final, period of the disease develop gradually due to the progressive nephrosclerosis. Low indices of clearance tests (especially insulin and PAH 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 of nitrogenous 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, in-dican) 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.

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

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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 (reserpin) 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, sour 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.

Prophylaxis. Prophylaxis consists in timely treatment of acute and chronic focal infections (tonsillitis, sinusitis, carious teeth, paradontosis, etc.). Patients with chronic glomerulonephritis should be regularly in­spected.

Toxic Kidney

Toxic kidney (acute nephrotic syndrome, acute nephrosis, necronephrosis) occurs in acute infectious and toxic diseases, such as typhus, malaria, influenza, ingestion of some nephrotoxic substances (corrosive sublimate, carbon tetrachloride), in transfusion of incom­patible blood, massive burns, and some other cases.

Pathological anatomy. In milder cases, insignificant dystrophy of epithelium of the prox­imal tubules occurs in the form of opaque swelling and fat infiltration in the tubular cells. In severe cases, the kidneys are slightly enlarged and flaccid. In poisoning with corrosive sublimate, the kidney is first red (large red kidney) due to pronounced plethora. Its vessels are then affected by the spasm and the kidney contracts (small white kidney). Histology reveals proteinous dystrophy and necrosis of the tubular cells and their desquamation; the glomeruli are often affected as well (acute necronephrosis).

Clinical picture. Symptoms of the disease vary greatly. Mild forms are practically asymp­tomatic; protein can only be detected in the urine. Febrile albuminuria occurring in infectious diseases can be used as an illustration. In severe forms of the disease, the urine excretion is upset, and oliguria develops. Hypertension and oedema are absent in typical cases. The urine is concentrated and its specific gravity is high; it contains protein, various casts, erythrocytes, cells of renal epithelium, and leucocytes. Renal dysfunction is aggravated by the disordered haemodynamics which attends shock (e.g. in burns, injuries). Anuria attends most severe cases; nitrogenous slags are accumulated in the blood. The patient dies within a few days unless excretion of urine is not restored.

Treatment. The main disease which is aggravated by the kidney affection should be treated. If oliguria or anuria persists, peritoneal dialysis or haemodialysis are indicated to pre­vent uraemia.

Amyloidosis of the Kidney (Amyloid Kidney)

Renal amyloidosis (amyloid nephrosis, amyloid dystrophy of the kidneys) is a manifestation of the general disease, amyloidosis.

Aetiology and pathogenesis. Congenital (hereditary), primary, and secondary congenital amyloidosis are distinguished. Secondary amyloidosis develops in the presence of pronounced protein metabolic disorders, mostly in patients with chronic inflammatory diseases such as tuberculosis, osteomyelitis, or bronchiectasis. Less frequently amyloidosis develops in deforming polyarthritis, lymphogranulomatosis, and some other diseases. It is believed that in all these diseases, in connection with chronic action of infection and toxins, and also decomposition of tissues and leucocytes, synthesis of proteins is distorted in the reticuloendothelial system. The auto-immune mechanism is actuated at a certain stage, and the production of antibodies to the altered own proteins is initiated. The antigen-antibody complexes, in the form of a specific firm amyloid substance, which is a combination of globulin and mucopolysaccharides, are deposited in various organs and first of all in the walls of fine vessels and capillaries under the argyrophilic membrane, under the tunica propria of the glands, and in the reticular stroma of various organs. Metabolism in

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the adjacent cells is upset due to deposition of amyloid. The cells and other tissue elements become compressed and atrophied. Genetically determined amyloidosis is the result of congenital defects of the enzyme systems responsible for the protein synthesis. Aetiology of sporadic primary amyloidosis is uncertain.

Pathological anatomy. Insignificant changes are found in the spleen, kidneys, liver adrenal glands, and the gastrointestinal tract (less frequently in lymph nodes and other organs) in amyloidosis. Amyloid kidneys are enlarged, consolidated, and grey (" large fatty kidney"). Histology reveals amyloid grains under the argyrophilic membrane of the arteries and capillaries. Capillary loops become obliterated, the glomeruli are replaced by amyloid grains or connective-tissue scars. Dystrophic changes in the tubular epithelium are also observed. Amyloid-affected (contracted) kidney is the result of a severe process.

Clinical picture. The clinical picture of all types of amyloidosis is the same. The clinical picture of secondary amyloidosis is largely determined by the main disease (pulmonary tuberculosis, osteomyelitis, etc.) and also (in all types of amyloidosis) by the degree of affection with amyloidosis of the other organs, e.g. the gastro-intestinal tract, the liver, the heart, and other organs and systems. Amyloid kidney usually occurs with the nephrotic syndrome (see " Nephrotic Syndrome"), which has its effect on the clinical picture of the disease. In the initial period of the disease the pa­tient's general condition is not affected. The study of the urine can only reveal proteinuria (to 10—15 g/1). As distinct from a " purely" nephrotic syndrome, the urine contains not only albumins but also globulins. Single casts (hyaline, granular, waxy, epithelial cells, leucocytes) can be found in the urinary sediment. The erythrocyte content is usually low, but some pa­tients have a pronounced nephrotic syndrome with typical changes in the urine.

The blood study reveals hypoproteinaemia with a specific prevalence of globulins (the albumin to globulin ratio decreases to 1.0 and more), and with the prevalence of a2- andy-globulins. Hypercholesterolaemia may also occur.

The differential diagnosis between amyloid kidney and other chronic diseases of the kidneys is often facilitated by the test with intravenous ad­ministration of Congo red. The method with subcutaneous injection of 1 ml of a 1 per cent methyl blue solution is commonly used. One-hour specimens of the urine are taken during 5 or 6 hours following administra­tion. Normally, all specimens should be coloured green. In the presence of amyloidosis, the colour changes insignificantly or does not change at all. But negative tests with Congo red or methylene blue do not rule out the presence of amyloidosis because the degree of affection may be insufficient to ensure reliable retention of the dye. An accurate diagnosis of amyloidosis can only be established by the results of nephrobiopsy.

Persistent oedema develops at later periods of the disease. Despite the affection of the renal vessels arterial hypertension is a rare symptom in amyloidosis. Glomerular filtration in patients with amyloid kidney becomes upset during the early period. At the final stage, a picture of pro­nounced renal failure arises; it is characterized by azotaemia and uraemia, from which the patient usually dies. Less frequently the patient dies of cachexia or other causes.

Treatment. Treatment of secondary amyloidosis can only be successful if the main cause of the disease is removed before severe changes have taken place in the organs, in the kidneys in the first instance. Treatment in­cludes a protein-rich diet (provided the nitrogen-excretory function of the kidneys is satisfactory) and containing limited quantity of sodium chloride; the therapy also includes vitamins and control of oedema and azotaemia (in the presence of renal failure).

Prophylaxis. It consists in timely revealing and treating chronic inflam­matory processes and purulent diseases to which amyloidosis is secondary.

Nephrolithiasis

Calculi are formed in the renal pelves in nephrolithiasis. The chemical composition of calculi is quite varied. They usually contain phosphates (calcium and magnesium salts of phosphoric acid). Less frequently calculi consisting of salts of oxalic acid (oxalates), uric acid (urates), and carbonic acid (carbonates) are encountered. Calculi may contain proteins, xanthine, cystine, and sulphonamide.

Aetiology and pathogenesis are uncertain. But it has been established that formation of calculi is stimulated by the infection of the urinary tract, injuries to the kidneys, and haemorrhages into the renal tissue, urinary congestion, and some avitaminoses (A, D). Metabolic disorders (hyper-parathyroidism) and sharp changes in the pH of the urine also promote calculi formation.

It is believed that precipitation of salts from the urine and calculi for­mation occur around an organic " nucleus" which may be desquamated cells of pelvic epithelium, accumulation of leucocytes, a blood clot, etc. But salts may precipitate if their concentration in the urine is increased or their solubility decreases due to changes in the pH of the urine, or if the concentration of the so-called protective colloids in the urine, which ensure stability of supersaturated solutions, decreases. For example, concentra­tion of the uric acid in the urine is usually 15—20 times higher than its solubility in water.

Clinical picture. The disease is characterized by attacks of nephrolithiasis (renal colic) which are followed by interparoxysmal periods.

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Most patients do not complain of anything in the interparoxysmal period. Only dull pain in the lumbar region occurs in some of them. The Pasternatsky symptom is as a rule positive. The study of the urine sometimes reveals transient haematuria; salt crystals are often found.

The first sign of the disease is usually an attack of renal colic, which develops during the passage of a calculus via the ureter. The attack occurs suddenly, often after jolting or long walking. The pain is localized in the lumbar region with radiation downward, by the course of the ureter, and into the sex organs. The pain is very severe and the patient is restless; he changes his posture continually. Pain intensity may lessen for a short time but then it intensifies even to a greater extent. The attack is attended by fre­quent and painful urination and various reflex symptoms (nausea, flatulence of the abdomen, retained stools). Erythrocytes and protein are found in the urine. The attack ends when the calculus passes into the urinary bladder. Sometimes the calculus passes the urethra and is excreted. Attacks recur at various intervals, from several attacks during one month to one during many years.

In the presence of typical attacks of renal colic, it is easy to diagnose nephrolithiasis. But it is sometimes difficult to differentiate renal colic in the right side from an attack of pain occurring in cholelithiasis. It should be remembered that pain in attacks of renal colic radiates downwards, whereas in attacks of hepatic colic it radiates upwards, into the right shoulder, shoulder blade, and the diuretic symptoms are absent. An attack of hepatic colic may end with jaundice.

Diagnosis in remission can be facilitated by X-ray examination (pyelography). The calculus can rarely be revealed on a survey X-ray pic­ture of the kidneys (Fig. 107). Oxalates, phosphates, and carbonates give an intense shadow on the X-ray patterns.

Course and complications. Long-standing presence of concrements in the renal pelvis has its specific effects: pyelitis (inflammation of the renal pelvis) usually develops, which can later transform into pyelonephritis (see " Pyelonephritis", below).

If a calculus is retained in the ureter to obliterate its lumen, the renal pelvis becomes distended by the accumulated urine to cause hydrops of the kidney (hydronephrosis) which causes future atrophy of the renal tissue. Pyonephrosis (acute purulent inflammation of the pelvis with involvement of the kidney tissue) develops if urine is infected. Pyonephrosis is characterized by a grave general condition of the patient, hectic fever with profuse sweating, dull pain in the corresponding side of the loin, neutrophilic leucocytosis with shift to the left, and markedly increased ESR.

Treatment. All measures should be taken to remove spasm and pain in

Fig. 107. Stones in both kidneys (scout radiograph).

attacks of renal colic. A hot-water bottle should be placed on the loin and atropine given subcutaneously. Hot water baths are also helpful. Procaine block in the lumbar region is given.

In the interparoxysmal period patients are recommended to drink much liquid. In the presence of urates, alkaline mineral water is desirable (Bor-zhomi, Essentuki mineral water). Great importance is given to the diet. Food rich in calcium chloride (milk, curd cheese, potatoes) and other substances that compose stones should be taken in limited quantity. In the presence of oxalates, green lattuce, beans, tomato and other foods contain­ing oxalic acid should be excluded from the diet. If urates are present, meat, fish and foods rich in purine bases should be ruled out.

If small stones are found in the pelvis, long walks, ample liquid intake, and antispasmodics containing essential oils (enathine, cystenal) should be prescribed to stimulate the excretion of the stones. If pyelonephritis joins the process, antibiotics and nitrofuranes should be given. Infected large stones should be removed surgically. This, however, does not eliminate the cause of stone formation and they can be formed again.

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Chapter 8. Urinary System

Pyelonephritis

ACUTE PYELONEPHRITIS

Aetiology and pathogenesis. Acute pyelonephritis arises as a result of infection spreading from the renal pelvis onto the kidney tissue in acute pyelitis, or as a result of infection of the kidney or its pelvis via haematogenic route in the presence of infectious foci in the patient's body (chronic tonsillitis, osteomyelitis). It may also develop during acute infec­tious diseases (acute tonsillitis, sepsis, typhoid fever, etc.). Penetration of the bacteria into the kidney and the pelvis does not always provoke acute pyelonephritis or focal nephritis: bacteriuria without symptoms of involve­ment of the renal tissue is often observed. Difficult urine outflow from the kidney (stone in the ureter, twisting of the ureter) stimulates development of pyelonephritis.

Pathological anatomy. The kidneys are slightly enlarged, the mucosa of the renal pelvis is inflamed and oedematous, ulceration is possible. If urine outflow is obstructed, the pelvis contains pus. Inflammatory infiltration of the renal tissue develops and purulent foci can be found in some parts of the kidney.

Clinical picture. The patient's condition is grave: high irregular fever, chills, dull lumbar pain. If inflammation spreads over onto the urinary bladder and the urethra, the patient feels tenesmus and sharp pain during urination.

Study of the urine reveals pyuria and bacteriuria. In complete obstruc­tion of the ureter and unilateral affection there may be no changes in the urine. Obliterated forms of acute pyelonephritis may also be observed (usually in the presence of grave general diseases). In such cases the kidney affection can only be suspected from the urinalysis.

Treatment. Antibiotics, sulpha and nitrofuran drugs (furadonin) are recommended.

CHRONIC PYELONEPHRITIS

Aetiology and pathogenesis. Pyelonephritis often arises in patients with chronic pyelitis due to transition of the inflammatory process from the renal pelvis onto the renal tissue. Nephrolithiasis facilitates fixation of the infection in the pelves and its spreading onto the renal tissue. Chronic pyelonephritis is usually caused by conventionally pathogenic flora, in­testinal escherichia; less frequently the disease is provoked by enterococ-cus, Proteus, or other infection. As infection spreads from the renal pelvis onto the renal parenchyma, the papillae are first affected, and then the

medullar and cortical layers of the kidney. The kidney contracts as a result. The process is often unilateral. If both kidneys are involved, the extent of affection may differ.

Clinical picture. Involvement of the renal tissue in the process alters the clinical picture of pyelitis to make it similar to that of chronic glomerulonephritis: hypertension develops, the concentrating and nitrogen excreting functions of the kidneys are gradually deranged, and uraemia develops. But as distinct from chronic glomerulonephritis, pyelonephritis is characterized by involvement of only one kidney or asymmetrical affec­tion of the kidneys. This can be revealed by intravenous or retrograde pyelography, separate study of the urine from the right and left kidneys ob­tained by catheterization of the ureters, and also by separate studies of some substances excreted by the kidneys. Clearance tests are useful, since they can reveal early signs of involvement of the distal tubules by the delayed excretion of phenol red and decreased excretion coefficient. Radiographic methods, such as renography and scanning, are also used for the purpose.

Pyelonephritis is characterized by the signs of infectious inflammation of the renal pelves, i.e. by the presence of bacteriuria, leucocyturia (especially the presence of active leucocytes known as Sternheimer-Malbin cells in the urinary sediment), and also deformation of the renal pelves as revealed by pyelography. Bacteriological study of the urine is of great significance: (cultivation of the urine on a nutrient media, and determina­tion of bacterial sensitivity to antibiotics). It should be remembered that urine specimens from women should only be taken by catheterization of the bladder. Differential diagnosis is facilitated by puncture biopsy of the kidneys.

At the terminal stage, due to involvement of both kidneys and develop­ment of nephrosclerosis, all functional tests for kidneys are not infor­mative. Death of patients is in most cases caused by uraemia.

Treatment. Infection is treated by antibiotics, sulpha drugs, and nitrofuran derivatives. Symptomatic therapy is given to control hyperten­sion and azotaemia (at the terminal stage).

Chapter 9. Diseases of the Blood

: Chapter 9. DISEASES OF THE BLOOD