impaired Serial estimations of plasma creatinine provide the best indication of the state of renal function

lupus erythematosus, anaphylactoid purpura. 2. Infections - Chronic pyelonephritis, renal tuberculosis. 3. Obstruction - Bilateral renal calculi, prostatic obstruction, urethral valves, retroperitoneal fibrosis. 4. Renovascular disease - Atheroma of renal arteries causing renal ischemia. 5. Interstitial nephritis. 6.Polycystic kidneys. B. SECONDARY RENAL DISEASE (Renal complication of systemic disease) 1. Diabetes mellitus. 2. Hypertension. C. IDIOPATHIC Pathogenesis-of clinical syndrome of CRF -1. Uremic toxins - Fall in glomerular filtration rate and reduction in renal tubular secretory capacity prevent certain substances from being excreted by the kidney and these probably produce their adverse effects on every organ of the body. However studies of the effects of dialysis, dietary modifications and transplantation have not identified the toxins involved. 2. Electrolyte and water excretion - Limited ability of diseased kidney to manipulate electrolyte and water excretion appropriately may lead to either salt and water retention with oedema and circulatory congestion, or to salt depletion. 3. Erythropoietin and 25-hydroxycholecalciferol -There is impaired production of erythropoietin and reduce hydroxylation of 25-hydroxycholecalciferol xycholecalciferol, the most active metabolite of vitamin D, a step which normally occurs in the kidney. 4. Renin - Impaired perfusion of remaining renal tissue may stimulate the inappropriate release of renin. 5. PTH - One of the principal disturbances of endocrine function in CRF is marked hyperplasia of parathyroid glands with very high levels of PTH. This contributes to renal oesteodystrophy, soft tissue calcification and bone necrosis in CRF, and also probably to pruritus, anemia, hypehipidemia, neurological disturbances and sexual dysfunction. However patients with primary hyperparathyroidism manifest few of these disturbances and the role of PTH in uremic toxicity is still uncertain. 6. 'Middle molecules' - The middle molecule hypothesis is based on the apparent absence of neuropathy in patients on chronic peritoneal dialysis (which is less efficient than hermodialysis in removing small molecules, but more efficient for middle molecules), and the high risk of neuropathy in patients treated with small surface area dialysers. Also the observation that when weekly hemodialysis time was markedly reduced, neuropathy did not appear provided a membrane highly permeable to middle molecules was used. While the identity of uremic toxins is largely unknown, it is suggested that some dialysis schedules permit accumulation in body fluids of molecules in the range 1,000 to 2,000 daltons, and these cause some of the uremic problems encountered by patients on regular dialysis. Stages - of chronic renal failure - 1 Diminished renal reserve -About 50-70% of kidney function has to be lost before the effect, on blood chemistry becomes readily detectable, e. g. , by rise of blood urea. 2. Renal insufficiency - from loss of further kidney function. There is moderate nitrogen retention (blood area 50-100 mg/100 ml., plasma creatmine 1.5-2.5 mg./100 ml.) and mild acidosis, may occur. Usually no symptoms except nocturia Hypertension may dominate the clinical picture. 3. Stage of renal failure - Further kidney damage produces considerable nitrogen retention, derangement of plasma electrolytes, anemia and usually marked symptoms. The term 'uremia' is reserved for the clinical syndrome resulting from advanced renal failure, when glomerular filtration rate is Management - 1. Monitoring renal functions - (a) Blood urea and creatinine - levels always raised. However normal levels cannot be taken to indicate that renal function is not impaired Serial estimations of plasma creatinine provide the best indication of the state of renal function in patients with CRF. Use of reciprocal plots of serum creatinine against time has shown that the decline in renal function is linear with time. An abrupt decline or acceleration in the slope demands a search for the cause (hypertension, UTI, hypovolemia or fluid overload, urinary tract obstruction particularly in elderly males, drugs or pregnancy). Hypercatabolic renal failure refers to rise of urea of more than 6.5 mmol/litre per day. (b) Ultrasound - to ascertain renal size and to monitor renal function regularly in patients with CHF who are prescribed ACE inhibitors (which may cause acute deterioration in renal function). 3. Plasma sodium -Hyponatremia is common. 4. Potassium - Normal values until terminal stages when hyperkalemia occurs. 5. Calcium, phosphate and magnesium - Increased plasma phosphate and decreased calcium levels. Magnesium levels normal or slightly raised. 6. Uric acid - increased. 7. Hypehipidemia - Raised plasma levels of triglycerides and pre-beta lipoproteins 8 Anemia - Normochromic normocytic anemia almost constant. Contributing factors - (a) Decreased production of erythropoietin by diseased kidney (ii) Direct marrow suppression by uremic toxins. (iii) Shortened red cell survival (iv) Increased blood loss 2 Conservative management of uremic syndrome - (a) Diet - Low protein diet of 40pg of protein (0.6g/kg). The diet must be high in essential amino acids and total caloric intake must exceed 35 kcal/kg/day, sing carbohydrate supplements if necessary. (b) Treatment of hyperkalemia - has already been described. 3. Salt and water intake - Salt overload and salt depletion are both hazards. The