Biomedical subjects
V Kher
Publications and source records attributed to V Kher.
The effect of aprotinin (a serine protease inhibitor) on renal function and renin release.
We studied the effect of aprotinin, a reversible inhibitor of kallikrein and other serine proteases, upon urinary kallikrein and kinin excretion, renal function and hemodynamics, blood pressure, and plasma renin activity (PRA). When aprotinin was administered to anesthetized rats at 10,000 KIU/kg as a bolus, and at 1000 KIU/kg/min infusion for 60 minutes, urinary kininogenase activity and immunoreactive kallikrein, kinins, sodium, potassium, and water excretion, and PRA decreased significantly. Aprotinin also caused a 36% decrease (p less than 0.001) in renal blood flow (RBF), and a 37% decrease (p less than 0.001) in glomerular filtration rate (GFR), although neither blood pressure nor cardiac output changed. The effect of aprotinin on PRA was further studied in conscious rats before and after stimulation of renin release by isoproterenol or furosemide. Aprotinin (5,000 KIU/kg bolus and 1000 KIU/kg/min infusion for 60 minutes) did not alter basal or isoproterenol-stimulated PRA, but it blunted the increase in PRA as stimulated by furosemide. Aprotinin at a higher dose (20,000 KIU/kg bolus and 5000 KIU/kg/min infusion for 60 minutes) significantly lowered blood pressure and increased hematocrit and PRA. These effects may be due to inhibition of serine protease(s) or to other as yet unrecognized properties of this peptide resulting from its highly cationic nature. In conclusion, aprotinin at a low dose decreased kallikrein, kinin, sodium, and water excretion. These decreases may be due to the inhibition of kallikrein and/or other serine proteases or may be secondary to the renal hemodynamic changes.(ABSTRACT TRUNCATED AT 250 WORDS)
Calcitropic hormonal status in north Indian patients with end-stage renal disease.
BACKGROUND: Bone disease in chronic renal failure has a wide spectrum that includes both high and low turnover conditions. Specific preventive and therapeutic measures require knowledge of the nature of bone involvement. Bone biopsy with static and dynamic histomorphometry is the gold standard for characterization of renal bone disease. However, non-invasive biochemical tests, especially serum intact parathyroid hormone (PTH), have a good correlation with histomorphometry. We studied the clinical and biochemical profile of bone disease in a sample of north Indian patients with chronic renal failure. METHODS: Twenty-nine patients of chronic renal failure were evaluated clinically, radiologically (subperiosteal erosions on hand X-rays) and biochemically (serum calcium, phosphorus, total alkaline phosphatase, intact PTH, osteocalcin, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D). Bone histomorphometry could be done in 4 patients. RESULTS: Serum intact PTH within or below the non-uraemic normal range, an index of low bone turnover, was seen in 17 (58.6%) patients. Serum osteocalcin, a bone formation marker, was within or below the non-uraemic normal range in 65.5% patients. Serum intact PTH and osteocalcin had a significant positive correlation (r = 0.6). Patient groups with clinical or radiological evidence of bone disease had serum intact PTH and osteocalcin levels comparable to those lacking such features. Serum intact PTH and total alkaline phosphatase were lower in haemodialysed (n = 25) patients than in those who had not received haemodialysis (n = 4). Low (< 10 ng/ml) serum 25-hydroxyvitamin D levels were seen in 7 (24%) patients while 1,25-dihydroxyvitamin D was low (< 15.9 pg/ml) in 20 (69%) patients. The biochemical parameters accurately reflected the bone histology (n = 4). CONCLUSIONS: Our data show that the majority of north Indian patients with chronic renal failure have biochemical evidence of low bone turnover. Empirical use of calcium salts and active vitamin D analogues without documentation of parathyroid status carry the risk of further suppression of bone turnover.
Acute renal failure in an intensive care unit in India--prognostic factors and outcome.
We prospectively analyzed 70 consecutive patients who developed acute renal failure (ARF) in the intensive care unit (ICU) during a six year period to define prognostic factors and outcome. Age, sex, preexisting chronic diseases, systemic infections, number of organs failing during the disease course, need and mode of renal replacement therapy (RRT), and length of stay in ICU were recorded. Analysis of factors in survivors (n=7, Gp A) and nonsurvivors (n=63, Gp B) was done by univariate and multivariate analysis. The mean age of patients was 28.6 years. Forty nine (70%) patients developed ARF following surgery, whereas 21 (30%) developed ARF in a medical setting. Cardiovascular surgery (39) and pancreatic surgery (7) were important causes in the surgical group, whereas in the medical group acute pancreatitis (11) was the main causative factor. One patient had ARF only, while in the rest, other organs were also involved. In more than 80% of these patients, organ failure and sepsis were present before the onset of ARF. Fifty two (74.3%) patients required dialytic support. The overall mortality was 90%. Number of organs failing, (1.5 +/-9 in Gp A vs 3.6 +/- 8 in Gp B), presence of systemic infection (1 in Gp A vs 55 in Gp B), prolonged stay in ICU (3.7 +/- 1.1 days in Gp A vs 8.0 +/- 5.4 in Gp B) and need for RRT (2 in Gp A vs 50 in Gp B) correlated with the mortality. Using multiple logistic regression analysis, only multiple organ failure (3 or more) correlated with the mortality. We conclude that multiple organ failure is a poor prognostic factor in patients with ARF in the setting of the ICU.
Wegener's vasculitis: diagnostic and therapeutic problems.
A case of Wegener's granulomatosis (WG) presenting with pulmonary manifestation which were initially suspected to be due to tuberculosis is being reported. Renal involvement appeared later. He developed complications of antitubercular treatment and of immunosuppression. The difficulties in distinguishing pulmonary manifestation of WG from tuberculosis and other diagnostic and therapeutic problems are discussed.