Renal thrombotic microangiopathy and cerebral venous thrombosis in a young man.

We report a patient of primary catastrophic antiphospholipid syndrome who presented with rapidly progressive renal failure and seizures. He was detected to have thrombotic microangiopathy on kidney biopsy and deep cerebral venous thrombosis. The patient was successfully managed with anticoagulants, steroids, plasmapheresis and cyclophosphamide.

Reversible segmental portal hypertension--an unusual presentation of abdominal tuberculosis in a renal transplant recipient.

Infections are the commonest cause of morbidity and mortality in renal transplant recipients. In India, tuberculosis is a one such common infection in these patients and presents with protean manifestations. We report here a case of pyrexia of unknown origin (PUO) and segmental portal hypertension in a renal transplant recipient. Search for the cause of portal hypertension revealed abdominal tubercular lymphadenitis. Treatment with anti-tubercular therapy caused regression of segmental portal hypertension.

Spectrum of renal lesions in HIV patients.

BACKGROUND: A variety of renal lesions have been reported in HIV positive patients from western world however there is paucity of Indian data. METHODS: Over a four year period, all hospitalised HIV positive patients were screened for renal involvement. Screening was done with urinalysis. Those with abnormality in urine examination underwent further assessment with clinical, biochemical, immunological profile and renal biopsy. Renal histology was studied by light and electron microscopy. RESULTS: Twenty-five (17.6%) of the 142 patients screened, had proteinuria/abnormal urinary sediment however none of the patient had proteinuria in nephrotic range. Fourteen of these 25 patients were asymptomatic while others had AIDS. Renal biopsy was studied by light microscopy in all and by electron microscopy in 11 cases. On histology mesangioproliferative GN was encountered in eight, focal segmental glomerulosclerosis in four and collapsing GN in one patient. In two cases cryptococcal infiltration and in one lymphomatous deposits were seen in glomerulus and interstitium. In one patient interstitium showed granulomas and in other three mononuclear cell infiltration. Histology was normal in 8 (32%) patients. On EM visceral cell hyperplasia and vacuolisation was seen in all, two had collapse of glomerular basement membrane and in three cases tubuloreticular structures were seen. There was no co-relation of renal histology with duration or severity of the disease (p > 0.05). No deterioration of renal function was seen over a short follow up period of 4.2 months (1-20 months). CONCLUSION: This study highlights that HIV patients exhibiting abnormal urinary sediment usually have underlying renal lesion and at times unexpected opportunistic infections may be present.

Hypochromic anaemia in chronic renal failure--role of aluminium.

BACKGROUND: Anaemia is a cardinal feature of chronic renal failure and classically it is normochromic normocytic. Hypochromic anaemia in these patients is often attributed to iron deficiency. AIM: This study was aimed to find the contribution of aluminium in causation of anaemia in CRF patients. METHODS: Dialysis dependent patients of chronic renal failure with adequate dietary intake (> 1500 Cals/day) and no apparent source of blood loss were evaluated for type of anaemia. (During period of this study centre didn't have reverse osmosis plant for water treatment). Evaluation included upper GI endoscopy, complete hemogram, serum proteins, serum iron, total iron binding capacity, and bone marrow iron status. For aluminium evaluation serum aluminium levels were done. RESULTS: Sixty-four patients were evaluated for type of anaemia. Mean age of patients was 41.19 years (15-76 years) with male:female ratio 2.3:1. Classical normochromic picture was seen in 28.5% while rest had hypochromic picture. On bone marrow aspiration study two patients had zero iron stores while all others had normal/excessive iron stores. In 10 patients with hypochromic picture, mean serum aluminium levels were 170 micrograms/L (30-310 micrograms/L). CONCLUSIONS: This study highlights the high prevalence of hypochromic anaemia in patients with adequate dietary intake and aluminium overload in Indian CRF patients.

Efficacy of enalapril in the treatment of steroid resistant idiopathic nephrotic syndrome.

Fifteen patients of idiopathic nephrotic syndrome who failed to respond to 8 weeks of corticosteroid therapy formed the material for this study. There were 10 males and 5 females, age ranging from 4 to 56 years. Three patients had hypertension. Histological lesions were focal and segmental glomerulosclerosis (FSGS) in 8; membranous glomerulonephritis in 3; mesangial proliferative glomerulonephritis in 2 and membranoproliferative glomerulonephritis in 2 patients. Proteinuria ranged from 3.64 to 8.66 g/1.73 m2/day. Serum albumin ranged between 2.2 to 3.3 g/dl. Serum creatinine was elevated > 1.5 mg/dl in 3 cases. After discontinuing steroids, enalapril was started in a dose of 2.5 mg/day and increased by 2.5 mg/day every 3-4 days till the maximum tolerated dose but not exceeding 20 mg/day. Proteinuria, serum albumin and serum creatinine estimations were done every 4 weeks for six months and every three months thereafter. Patients were followed up for 6 to 30 months. Proteinuria decreased to < 1.5 g/1.73 m2/day in 12 patients (80%) and to < 0.5 g/1.73 m2/day in 10 patients (66.7%) by 8 weeks. There was no significant decrease in proteinuria in 3 (20%) patients; two of these were cases of FSGS and one of membranoproliferative glomerulonephritis. Oedema, hypoalbuminaemia and hypercholesterolaemia returned to normal in all patients who had a decrease in the proteinuria. There was no correlation between the histological lesion and response to enalapril. There was no rise in the serum creatinine level above the baseline in any of the patients. Except for cough in one patient, no other significant side effects were observed. We conclude that enalapril is effective in reducing proteinuria and thereby the morbidity in steroid resistant nephrotic syndrome irrespective of the underlying pathology.

Invasive pulmonary aspergillosis and nocardiosis in an immunocompromised host.

A case of invasive pulmonary aspergillosis and nocardiosis following high dose prolonged steroid therapy given for suspected rapidly progressive glomerulonephritis is reported. A favourable response was achieved with a combination of amphotericin B and cotrimoxazole. A high index of suspicion and aggressive investigations are necessary for confirmation of diagnosis and early institution of appropriate therapy.