Acute interstitial nephritis due to endosulfan.
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Biomedical subjects
Publications and source records attributed to M Segasothy.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
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Two-hundred and sixty-five patients with asymptomatic proteinuria and/or haematuria were studied at the Department of Medicine, Universiti Kebangsaan Malaysia and Department of Nephrology, General Hospital Kuala Lumpur. They represented 25.4% of all the renal biopsies performed during the period 1980-88. All the three races were affected with 71.3% occurring between the ages of 20-39 years and 41.1% were detected during routine medical examination. Excluding those patients with lupus nephritis, IgA nephropathy was the commonest histological diagnosis (51.7%). The presence of severe and advanced histological changes in a significant number of biopsies emphasises the need for more effective screening and early referral of this group of patients.
A total of 164 patients with IgA nephropathy were diagnosed at the Department of Medicine, Universiti Kebangsaan Malaysia and the Department of Nephrology, General Hospital, Kuala Lumpur between 1981-1988. This represented an incidence of 20.1% of all primary glomerulopathies seen in both units. The 3 major ethnic groups were equally affected with 59.7% occurring between the ages of 20-36 years. It was not uncommon in females. The high prevalence of hypertension, renal failure, heavy proteinuria at presentation and the increased chronicity index in the biopsy, suggest that IgA nephropathy is progressive disease leading to chronic renal failure.
We report two cases of acute renal failure that followed the ingestion of jering. Features of jering poisoning included clinical presentation of bilateral loin pain, fever, nausea, vomiting, oligo-anuria, haematuria and passage of sandy particles in the urine. Blood urea (40.8 mmol/l; 21.9 mmol/l) and serum creatinine (1249 mumols/l; 693 mumols/l) were markedly elevated. With conservative therapy which included rehydration with normal saline and alkalinisation of the urine with sodium bicarbonate, the acute renal failure resolved.
Six hundred and one intravenous Urograms (IVU) done at the General Hospital, Kuala Trengganu from 1981 to 1985 were reviewed retrospectively for Renal Papillary Necrosis (RPN). It was found that 1.3% of IVUs had RPN. There was a higher incidence of RPN amongst males as compared to females. RPN occurred more commonly in the younger age groups.
Controversy exists as to the type of cells present in the urine during renal allograft rejection. In order to resolve this controversy as well as to evaluate the value of urine sediment examination as a means of detecting AR, we quantitated the different cells present in urine during AR using an immunoperoxidase technique and monoclonal antibodies reactive with lymphocytes, monocytes, granulocytes, glomerular epithelial, tubular, and urothelial cells. Urine sediment (n = 176) was examined serially over 3 months in 15 transplant recipients. There were 12 episodes of early posttransplant acute tubular necrosis and 21 episodes of AR. It was possible to detect AR as well as to distinguish AR from ATN. Lymphocyte and tubular cell excretions were increased significantly during AR. Excretion of urothelial cells was also significantly increased during most episodes of AR suggesting that rejection of ureters occurs concomitantly with rejection of the kidneys.
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Nucleated nonsquamous cells in urine of patients with crescentic glomerulonephritis (CN), noncrescentic glomerulonephritis (NCN), acute tubular necrosis (ATN) and drug related acute interstitial nephritis (AIN) were identified using monoclonal antibodies and immunoperoxidase stain. Cell viability was determined by trypan blue permeability. CN was distinguishable from NCN by total cell numbers exceeding 30,000/ml (p less than 0.001) and counts of granulocytes exceeding 10,000/ml (p less than 0.05), monocytes exceeding 3,000/ml (p less than 0.001), T4 lymphocytes exceeding 1,500/ml (p less than 0.001), T8 lymphocytes exceeding 1,500/ml (p less than 0.001), glomerular epithelial cells exceeding 4,000/ml (p less than 0.001), proximal tubular cells exceeding 8,000/ml (p less than 0.001), loop of Henle cells exceeding 1,500/ml (p less than 0.01) and urothelial cells exceeding 1,500/ml (p less than 0.05). AIN was distinguishable from ATN by total cell numbers exceeding 75,000/ml (p less than 0.001) and counts of granulocytes exceeding 150,000/ml (p less than 0.001), monocytes exceeding 5000/ml (p less than 0.001), T4 lymphocytes exceeding 3,000/ml (p less than 0.01), T8 lymphocytes exceeding 2,500/ml (p less than 0.01) and cell viability exceeding 60% (p less than 0.05). Proximal tubular, loop of Henle, distal tubular/collecting duct and urothelial cells were present in high numbers in CN, ATN and AIN. CN can be distinguished from NCN, and ATN can be distinguished from AIN by identifying and quantifying the nucleated cells present in the urine.
A method to identify nucleated nonsquamous cells in urine using monoclonal antibodies and immunoperoxidase stain is described. Cells from washed deposits of midstream urine samples were transferred to gelatinized slides in a cytocentrifuge, air-dried, acetone fixed, and subjected to microwave irradiation. Slide preparations were then treated with monoclonal antibodies with the use of a four-layer peroxidase-antiperoxidase technique. It was possible to identify granulocytes, monocytes, lymphocytes, and renal epithelial and urothelial cells. This method was found to be helpful in determining the profiles of cells in urine in acute tubular necrosis, drug-related acute interstitial nephritis, and crescentic glomerulonephritis.
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180 patients with end-stage renal disease (ESRD) on maintenance dialysis and those who had undergone renal transplantation were questioned retrospectively. 14 patients had consumed excessive quantities of analgesics (greater than 1 kg) prior to the institution of long-term dialysis or transplantation. Sonographic examination done on these patients indicated that 7 had renal papillary necrosis (RPN). The sonographic features were renal papillary calcifications surrounding the central sinus in a complete or incomplete garland pattern. In 5 of these patients RPN is attibutable to the excessive consumption of paracetamol. We have earlier reported 10 cases of RPN due to excessive consumption of paracetamol. Thus 15 cases of RPN attributable to paracetamol consumption (1.0-15.3 kg over a period ranging from 3 to 23 years) have been documented. It is concluded that paracetamol may assume an increasingly important role in the causation of analgesic nephropathy (AN) and ESRD.
Accurate identification of nucleated cells in urine can be difficult with conventional methods of microscopic urinalysis. Monoclonal antibodies were used with an immunoperoxidase technique to identify nucleated cells in urine. This new development in urinalysis is in its early stages, but it has helped to circumvent the difficulties associated with standard microscopy. The monoclonal antibody technique allowed for the identification of granulocytes, monocytes, lymphocytes, glomerular epithelial, proximal tubular, loop of Henle, distal tubule/collecting duct, and urothelial cells in urine, and by quantifying these cells it was possible to determine the urine cell profiles in various renal diseases as well as in allograft rejection and early post-transplant acute tubular necrosis in renal allograft recipients. The cell profiles are useful in aiding the diagnosis of these conditions.
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