M.G. Kirubakaran

Terminal Infections in Renal Transplant Patients in a Tropical Environment

Infections were a major cause of death in 84% of 38 autopsied renal allograft recipients in a south Indian hospital. Pyogenic bacteria and fungi were the most common etiological agents encountered, being present in 50 and 47% of cases, respectively. Tuberculosis and hepatitis B virus infection were more prevalent and Pneumocystis carinii and cytomegalovirus disease rarer than in comparable series from non-tropical countries. 1 case each of amoebiasis, strongyloidiasis and filariasis were the parasitic infections encountered.

Acute eosinophilic glomerulonephritis with Bancroftian filariasis

A case is reported of Bancroftian filariasis and acute immune complex glomerulonephritis in a 44-year-old man. Renal biopsy showed microfilariae and large numbers of eosinophils in the glomeruli (eosinophilic glomerulonephritis). The absence of other aetiological factors suggests that the glomerulonephritis may have been of filarial origin.

Presentation, prognosis and outcome of IgA nephropathy in Indian adults

Background:  IgA nephropathy (IgAN) is not well characterized in India. This retrospective study of 478 patients with IgAN was performed to clarify the presenting features, prognostic factors and the renal survival rates of the disease.

Minimal-Change Nephrotic Syndrome in Adults Treated with Alternate-Day Steroids

Fifty-eight previously untreated adults with minimal-change nephrotic syndrome (MCNS), who had a mean follow-up period of 35.8 months, were studied with regard to their response to alternate-day steroid therapy. The nephrotic syndrome in 54 patients (93%) remitted by 12 weeks and patients continued to be in remission at 16 weeks. Of the 54 patients, 8 (14.8%) had frequent relapses and 9 (16.6%) had infrequent relapses. No serious complications as a result of steroid therapy were encountered.

Prediction of mortality in acute renal failure in the tropics.

Despite significant improvements in medical care, acute renal failure (ARF) remains a high risk for mortality. It is important to be able to predict the outcome in these patients in view of the emotional and ethical needs of the patients and to address questions of efficiency and quality of care. We analyzed the risk factors predicting mortality prospectively in a group of 265 patients using univariate and multiple logistic regression analysis. A prognostic model was evolved that included 10 variables. The model showed good discrimination [(receiver operating characteristic (ROC) area = 0.91) and correctly classified 88.30% of patients. The variables significantly associated with mortality were coma odds ratio (OR) = 9.8], oliguria (OR = 4.9), jaundice (OR = 3.7), hypotension (OR = 3.1), assisted ventilation (OR = 2.3), hospital acquired ARF (OR = 2.3), sepsis (OR = 2.2), and hypoalbuminemia (OR = 1.7). Age and male gender were included in the model as they are clinically important. The score was validated in the same sample by boot strapping. It was also validated in a prospective sample of 194 patients. The model was calibrated by the Hosmer-Lemeshow goodness-of-fit test. It was compared with two generic illness scores and one specific ARF score and was found to be superior to them. The model was verified in different subgroups of ARF like hospital acquired, community acquired, intensive care settings, nonintensive care settings, due to sepsis, due to nonsepsis etiologies, and showed good predictability and discrimination.

Haemolytic-uraemic syndrome complicating snake bite.

Anand Date, MD, Professor of Pathology, Christian Medical College Hospital, Vellore 632004, Tamil Nadu (India) Dear Sir, The triad of acute renal failure (ARF), thrombocyto-penia and haemolytic anaemia with fragmented erythrocytes (schistocytes) comprise the haemolytic-uraemic syndrome (HUS) [1]. In addition to its primary idiopathic childhood form, this syndrome can occur secondarily with viral and bacterial infections, oral contraceptive use and in pregnancy and in the puerperium [2]. Its occurrence after snake bite is not well known. During the period 1975–1983, 12 female and 12 male patients, with a mean age of 36 years (SD 14 years), were treated for ARF following snake bite at the Christian Medical College Hospital at Vellore in southern India. They had been referred for treatment from peripheral clinics 2–21 days after the onset of oliguria. Initially the patients had severe pain and swelling at the site of the bite and bleeding manifestations, most commonly haematu-ria with prolonged bleeding and clotting times. Oliguria or anuria developed within 24 h of the bite, and lasted for 4–47 days. The snake was identified by description as Vipera russelli in 7 cases. In the remainder, identification could not be made, although the symptomatology suggested that the Russell’s viper was involved in all cases and this is the only snake in this region whose bite is reported to cause ARF [3]. Results of laboratory investigations were as follows: Blood urea, mean 46.5, SD 25 mmol/l; plasma creati-nine, mean 967, SD 417 μmol/l; platelet count, mean 104, SD 92 × 10V1; packed cell volume, mean 0.27, SD 0.11; reticulocyte count, mean 5, SD 3%; total leukocyte count, mean 13.3, SD 4× 10V1; differential neutrophil count, mean 80, SD 8%. Schistocytes were present in the peripheral blood smears of 22 patients. Sixteen patients had HUS with anaemia, schistocytosis and thrombocyto-penia. Six patients had normal platelet counts when first examined 7 days or more after the bite, and there was no record of schistocytes in the peripheral blood smear in 2 cases. Absence of the complete triad could, in most cases, be attributed to incomplete or delayed investigation. Percutaneous renal biopsies performed in 15 patients showed cortical necrosis in 3 cases and acute tubular necrosis in the rest. Fibrin and platelet clusters were demonstrable in glomeruli and small calibre blood vessels in 5 of the 7 biopsies examined electron microscopically [4, 5]. Two patients were treated conservatively, 2 with hae-modialysis and the rest by peritoneal dialysis. One patient died of massive haematemesis soon after admission to hospital. Patients with cortical necrosis developed chronic renal failure, the others made a complete recovery.

Central nervous system disease in renal transplant recipients.

Anand Date, MD, Professor of Pathology, CMC Hospital, Tamil Nadu (India) Dear Sir, Diseases of the central nervous system (CNS) are an important cause of morbidity and mortality in renal transplant recipients [1]. Since there are few reports reviewing these lesions, we describe here the CNS complications that occurred in 38 of the 550 patients who received live-donor renal allografts at our centre during a 15-year period. The findings and methods of diagnosis are summarised in table I. As expected from other reports [1–3], infections were the commonest CNS complications, being seen in cases 1–16. However, tuberculous meningitis was much more frequent reflecting the higher prevalence of tuberculosis in the tropics. Case 4 who died of gram-negative bacillary septicaemia had microglial nodules in the pons; such lesions have been reported previously and are believed to be due to cytomegalovirus or herpes simplex virus infection [3, 4]. Cryptococcus was the fungus most frequently involving the CNS, though it is uncommon among all systemicfungal infections in suchpatients here [5]. Cerebrovascular accidents occurred in cases 17–25 including 8 of the 283 renal transplant recipients treated using a high-dose steroid schedule employed earlier and in only 1 of the 267 cases who were given steroids according to the newer low-dose regimen. This difference was statistically significant by Fisher’s exact test (p < 0.02). All these patients had hypertension and 2 had diabetes mellitus as well. Eight patients presented with convulsive disorders, of whom 4 had hypertensive encephalopathy and 2 idio-pathic epilepsy. Patients 30 and 31 had generalised convulsions with serum calcium levels of 0.95 and 1.05 mmol/l, respectively. Detailed investigations failed to reveal any cause for hypocalcaemia, but both patients improved with calcium supplements. All 3 patients with hepatic encephalopathy had HBs antigenaemia. Case 37 developed drowsiness 5 months after transplantation, at which time renal functions were only mildly impaired and other investigations including cerebrospinal fluid examination were normal. A CAT scan and EEG showed evidence of bilateral frontal lobe atrophy of unknown cause. Extensive investigations including a diagnostic laparotomy failed to show the cause of fever in case 38, but necropsy revealed pulmonary nocardiosis and central pontine myelinolysis

Medical Renal Disease in the Elderly in a Southern Indian Hospital

A review of 85 patients aged 60 years or more, treated in a southern Indian hospital for conditions requiring renal biopsy, showed that diffuse poliferative glomerulonephritis was the most frequent diagnosis, being present in 24 cases of whom 11 had elevated serum streptococcal antibody titres. Infections were also important in 2 patients with amyloidosis secondary to tuberculosis, in 3 patients with acute tubular necrosis following infectious gastroenteritis and in a patient with acute pyaemic interstitial nephritis with septicaemia. Drugs including indigenous medicines were the other important cause of renal disease, being implicated in 11 cases.

Renal Histology for the Diagnosis of Primary Hyperoxaluria in Patients with End-Stage Renal Disease

Prof. J.C.M. Shastry, Department of Nephrology, C.M.C. Hospital, Vellore 632004 (India) Sir, Renal transplantation is no longer contraindicated in patients with end-stage renal disease (ESRD) due to primary hyperoxaluria. Recurrence of the disease in the graft can be prevented by special preand posttransplan-tation measures [1]. Hence, it is important to establish the diagnosis of primary hyperoxaluria before transplantation. The diagnosis of primary hyperoxaluria in ESRD is difficult by current methods as it depends on the demonstration of increased urinary oxalate excretion [2], In advanced renal failure urinary oxalate excretion decreases and may fall within normal range. The plasma oxalate levels vary widely [2]. Furthermore, oxalate deposits can occur in kidneys of patients with ESRD due to diseases other than primary hyperoxaluria [3, 4]. The present study was undertaken to determine whether the magnitude of oxalate deposition in kidneys of patients with ESRD would be useful in the diagnosis of primary hyperoxaluria. Pretransplant nephrectomy specimens in 41 patients with ESRD were studied. Of these 2 patients had primary hyperoxaluria. The etiology of ESRD in the remaining 39 patients was uncertain: end stage histology in 19, chronic interstitial nephritis in 8, adult polycystic kidney disease in 6, chronic glomerulonephritis in 4 and end-stage of crescentic glomerulonephritis in 2. The histological sections of these nephrectomy specimens were reviewed. Clinical information was obtained from the hospital records. The average duration of dialysis was 4.2 months (range 1–7 months). Calcium oxalate crystals were identified as light brown crystals in hematoxylin-eosin sections. Using polarized light, oxalate deposit was quantified. Ten non-overlapping cortical fields were examined and the number of tubule cross-sections containing oxalate crystals were counted and scored according to the method of Scheinman et al. [1]. Microscopically oxalate crystals were deposited most commonly in tubules (fig. 1, 2). Interstitial oxalate crystals were less frequently seen. Fig. 1. Renal oxalate deposits in ESRD not due to hyperoxaluria. Fig. 2. Renal oxalate deposits in ESRD due to primary hyperoxaluria.

Nephrotic-Range Proteinuria with Renal Artery Stenosis: Its Reversal after Transluminal Angioplasty

Dr. S. Hariharan, Department of Nephrology, CMC Hospital, Vellore 632004 (India) Dear Sir, Nephrotic-range proteinuria secondary to renal artery stenosis is known [1, 2]. Decrease in the proteinuria has been reported after nephrectomy [2, 3]. Its reversal after transluminal angioplasty is documented below: A 14-year-old girl presented for evaluation of hypertension and albuminuria. Her blood pressure was 200/120 mm Hg in the supine position and 170/110 mm Hg when erect. There was no pedal edema and no flank or abdominal bruit; laboratory tests showed qualitative urine protein 4 + , blood urea 25 mg/dl, serum creatinine 1.2 mg/dl, urine protein excretion 3.4 g in 24 h, total serum protein 6.7 g/dl, serum albumin 4.1 g/dl, serum sodium 139 mEq/1, potassium 3.3 mEq/1, bicarbonate 20 mEq/1 and chloride 102 mEq/1. There was no serological evidence of systemic lupus erythematosus. Renal histology was normal on light-microscopy and immunofluo-rescence study. A renal angiogram revealed bilateral renal artery stenosis. Blood pressure was controlled with a combination of α-methyl-dopa 500 mg, hydralazine 50 mg, clonidinie 0.1 mg and nifedipine 10 mg given 8-hourly together with frusemide 40 mg once a day. Following transluminal angioplasty, blood pressure was controlled by hydralazine 50 mg three times daily alone. The excretory function of both kidneys, as shown by intravenous urogram, had improved after angioplasty, and 24-hour urine protein excretion was only 975 mg 7 days after the procedure and the qualitative proteinuria was 1 + ‚ 7 months after the procedure. References Berlyne, G.M.: Tavill, A.S.: C. Baker, S.B de: Renal artery stenosis and the nephrotic syndrome Q. Jl Med. 33: 325-335 (1964). Montoliu, J.; Botey, A.; Torras, A.; Darnell, A.; Revert, L.: Renin-induced massive proteinuria in man. Clin. Nephrol. 11: 267-271 (1979). Eiser, A.R.; Katz, S.M.; Swartz, C: Reversible nephrotic-range proteinuria with renal artery stenosis: clinical example of renin-associated proteinuria. Nephron 50:374-377 (1982).