Biomedical subjects
Publications and source records attributed to H S Uberoi.
A patient who developed hypopituitarism after viperine envenomation is described. Thrombosis as a part of disseminated intravascular coagulation may have been the cause. Hypopituitarism should be suspected in such cases especially when there is associated acute renal failure.
During the last 6 years, 7 healthy individuals who were reasonably well acclimatised to physical exertion came under observation with acute renal failure due to exercise induced myoglobinuria. Their mean age was 20 years, and renal failure resulted after cross country run of 10-15 km in 6 cases and long route march of 90 km in 3 days in one case. There was no evidence of effects of heat, dehydration or hypotension. Apart from myoglobinuria and significant urinary sediments, serum aldolase (mean 69.0 SL u/ml) and serum creatinine phosphokinase (mean 120.0 Sigma u/ml) were also elevated. Maximum blood urea and creatinine were 224 mg/dl and 13.9 mg/dl respectively. Hypocalcaemia was noticed in 3 cases, hyperkalaemia in 4 cases and hyperuricaemia in one case during the oliguric phase. One case had features of non-oliguric acute renal failure. All cases recovered though 4 cases required dialysis support. Kidney biopsy in 3 cases showed recovering acute tubular necrosis with eosinophilic material in tubules. Lactate studies in the convalescent period revealed normal response and repeat physical exertion of same severity after 6 months did not reproduce the syndrome. It is concluded that exertional rhabdomyolysis unassociated with heat stress is a rare entity, and with prompt diagnosis and energic management results are rewarding.
Twenty five cases with systemic lupus erythematosus admitted to a referral service hospital over a period of 6 years have been studied to analyse the pattern of multisystem involvement. Febrile polyarthritis, renal involvement and skin changes dominated the clinical picture. Important serological abnormalities included the presence of antinuclear antibody and anti ds DNA. Renal biopsy carried out in all cases helped to reveal lupus nephritis in subclinical cases. The pattern of renal involvement varied, with diffuse proliferative glomerulonephritis being the commonest. Oral steroids was given to all cases and cyclophosphamide was given to severe and resistant cases. The severity of system involvement, especially renal, influenced the response to treatment. Changes in presentation between Indian and Western patients are highlighted.
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The incidence of renal vein thrombosis (RVT) and other thrombo-embolic phenomena was evaluated in 44 unselected patients with nephrotic syndrome. Renal vein thrombosis was demonstrated by selective renal venography in 10 patients and at post-mortem in one. Extension of the thrombus from the renal veins into the inferior vena cava was seen in 3 patients. Evidence of thrombo-embolism elsewhere in the body was seen in the form of thrombophlebitis in the lower extremities in 4 patients (9.1%), pulmonary embolism in 3 (6.8%) and myocardial infarction in one (2.3%). Of the 11 patients with RVT, renal histology showed membranous glomerulonephritis in 3, minimal change nephritis in 5, membrano-proliferative in one and focal and diffuse proliferative glomerulonephritis in one patient each. The characteristics clinical findings such as gross haematuria and flank pain were noted in only 3 patients with RVT. No significant difference could be detected between the plasma fibrinogen, serum cholesterol, beta-lipoprotein, triglycerides and phospholipid concentration of those who showed RVT and the remainder in whom RVT was not demonstrated. The possible mechanisms involved in the pathogenesis of RVT in nephrotic syndrome are discussed.
A case of acute renal failure after mercuric chloride poisoning is reported. Laboratory data revealed markedly elevated serum concentrations of aldolase and creatine phosphokinase, and the presence of pigment granular casts and myoglobin in the urine. The patient went into a diuretic phase after 12 days of oliguria and renal function returned to normal during the next 10 days. Besides direct nephrotoxicity, the contributory role of rhabdomyolysis in the pathogenesis of renal failure after mercuric chloride poisoning, has been stressed.