Diabetes mellitus, amyloidosis, SLE, Henoch-Schonlein Purpura, cryoglobulinemia, polyarteritis nodosa

as dipyridamole because of involvement of coagulation process in crescent formation, 3, CHRONIC GLOMERULONEPHRITIS CLINICAL FEATURES (a) Persistent proteinuria - After an apparent recovery from attack of acute nephritis or asymptomatic proteinuria discovered at routine examination. After a variable period of upto 20 years, hypertension and renal failure supervene (b) Nephrotic syndrome - About half the patients who develop chronic glomerulonephritis pass through a nephrotic phase with hypoalbuminemia, oedema and massive proteinuria. (c) Persistent hematuria - Hematuria begins with onset of sore throat and may last several weeks No oedema or hypertension. In between attacks patient is well. Many patients also have persistent proteinuria. (d) Chronic renal failure - Final stage. In majority the symptoms of advanced chronic renal failure, hypertensive cardiac failure, or malignant hypertension are the first indication of its presence. Symptoms and signs of uremia - nausea, vomiting, hiccough, fatigue, anaemia (normochromic, normocytic); dyspnoea, pruritus, pericarditis, bloody diarrhoea, nocturia Often the only symptom before the onset of uremia is nocturia for a period of months or years. DIFFERENTIAL DIAGNOSIS -1 Essential hypertension - No history of AGN, patient not pale or inert. No anemia, no oedema of feet. B.P. more labile No or slight impairment of renal function. 2. Chronic pyelonephritis - (a) Urine culture shows organisms though these may appear intermittently. (b) History of recurrent rigors and fever, often with loin pains. (c) Urinary excretion of white cells much more than of red cells. (d) Pyelography will show distortion of the pelvicalyceal pattern. 3. Renal tuberculosis - should be considered in any patient with unexplained genitourinary symptoms or persistent symptomless albuminuria, pyuria or microhaematuria Positive culture or other diagnostic techniques. Excretory urograms may be normal in the presence of minimal disease or may reveal changes suggestive of tuberculosis such as incomplete visualization of one or more calyces, a fuzzy outline of a calyx, a cavity, hydronephrosis or nonvisualization of the entire kidney. Cystoscopy may demonstrate diffuse cystitis, tubercles, ulcerations or 'golf-hole1 ureters. 4. Polyarteritis nodosa - Hypertension and renal failure with often arthropathy, neuropathy and pyrexia 5 Systemic lupus erythematosus - may present with renal involvement. The commonest finding is persistent symptomless proteinuria usually accompanied by microscopic haematuria. 6. Polycystic kidneys - Hypertension, cardiac hypertrophy, haematuria and renal insufficiency simulate chronic nephritis. Palpable kidney tumours and diagnosis by radiology MANAGEMENT - (i) Control of hypertension with suitable hypotensive agents. (ii) Treatment of anaemia by blood transfusion (iii) Low protein diet. (iv) Dialysis (See treatment of chronic renal failure). SALT-LOSING NEPHRITIS - As the glomerular filtration rate (GFR) falls, the remaining living nephrons undergo osmotic diuresis and the loss of sodium in urine causes salt-wasting' or salt-losing nephritis' The common causes of salt-losing nephritis are: (a) Chronic renal failure. (b) Pyelonephritis. (c) Addisons disease. This can be treated by careful resalination by giving 250 ml. of 3 percent sodium chloride. 4. NEPHROTIC SYNDROME (NS) - Definition - A clinical condition in which there is oedema, proteinuria and hypoproteinemia irrespective of etiology or any other additional abnormal clinical features. Over 80% of patients with nephrotic syndrome have idiopathic glomerular lesions Causes - 1. Primary glomerular diseases - (a) Minimal change nephropathy (b) Mesangioproliferative glomerulonephritis (c) Membranous nephropathy. (d) Focal and segmental glomerulosclerosis. (e) Crescentic glomerulonephritis. 2. Idiopathic 3 Secondary to other diseases - (a) Infections - Malaria, hepatitis B, herpes zoster, streptococcal and staphylococcal infections, syphilis, leprosy, schistose miasis. (b) Drugs - Heavy metals such as gold, anticonvulsants (especially phenytoin andtroxidone), penicillamine, ACE inhibitors, heroin, rifampicin NSAIDs, tolbutamide and probenecid. (c) Tumours - Carcinoma, leukemia and lymphoma, multiple myeloma. (d) Systemic diseases - Diabetes mellitus, amyloidosis, SLE, Henoch-Schonlein Purpura, cryoglobulinemia, polyarteritis nodosa. (e) Familial disorders - Congenital (neonatal) nephrotic syndrome. Airports syndrome, Fabrys disease. (f) Miscellaneous conditions - Reflux nephropathy, renal vein thrombosis, toxemia of pregnancy, allergic reactions to insect bites, pollens and vaccines, renal artery stenosis. Pathology - The kidneys are large, pale and soft. Biopsy studies show a wide variety of histopathological changes - (a) Minimal change nephropathy is common in very young children (b) Focal glomerulosclerosis. (c) Membranous nephropathy. (d) Proliferative glomerulosclerosis - accounts probably for the largest group of adults with idiopathic nephrotic syndrome. Clinical features - 1. Age and sex - Two to three times more common in childhood with peak incidence at 2-3 years In this age group there is a male female ratio of 2.5:1, in adults, sex incidence is equal. 2. Oedema - Oedema is peripheral involving the limbs, particularly lower limbs. In children oedema may be more obvious in