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M S Parmar

Publications and source records attributed to M S Parmar.

8 recordsLinked to original sources
PubMed1998

Studies on the pathogenesis of hypokalemia in Gitelman's syndrome: role of bicarbonaturia and hypomagnesemia.

OBJECTIVE: Hypokalemia and renal potassium (K) wasting are hallmarks of the group of disorders called Bartter's syndrome. The presence of hypomagnesemia and a low rate of excretion of calcium are currently used to characterize a subgroup of these patients as having Gitelman's syndrome (GS) in which the molecular lesion is a defect in the thiazide-sensitive NaCl cotransporter in the distal convoluted tubule. This study was undertaken to examine whether bicarbonaturia or hypomagnesemia exacerbates the kaliuresis in patients with GS. METHODS: Six patients with most of the diagnostic features of GS were examined. To examine the role of bicarbonaturia, the transtubular K concentration gradient (TTKG) was assessed before and after an oral load of NH4Cl which caused the urine pH to be < 6. To evaluate the role of hypomagnesemia, the TTKG was examined after an infusion of enough magnesium (Mg) to achieve normal levels of Mg in plasma for close to 24 h. RESULTS: The TTKG remained very high even when the pH of the urine was < 6.0. An infusion of Mg caused the TTKG to approach expected values for hypokalemia in 4 of 6 patients. The infusion of Mg was extended in 1 patient who had a sustained high TTKG for 24 h; the TTKG remained elevated for 96 h despite normal plasma Mg levels. CONCLUSIONS: Bicarbonaturia does not play a critical role in maintaining the very high TTKG in these patients. The K wasting in 4 of 6 of these patients could largely be attributed to hypomagnesemia and/or Mg depletion. The plasma aldosterone level tended to be higher in patients who did not respond to the infusion of Mg. Therefore, these patients may not represent a homogeneous group with regard to the pathophysiology of their renal K wasting.

Adult↗
PubMed1998

Killer dreams.

Emotional stress is a recognized trigger for coronary artery spasm. An association between dreams and sudden death is described in folklore and medical history, and originates from the common experience of being awakened by vivid, frightening dreams, with racing pulse, cold sweats and other physiological responses associated with intense distress. Intense alterations in autonomic activity during dreaming can have dire consequences in patients with cardiovascular disease. Four patients with no evidence of underlying coronary artery disease, where emotional stress produced by nightmares or 'deadly dreams' caused coronary artery dissection in two and vasospasm in the other two, leading to life-threatening cardiac events, are presented. A possible mechanism is speculated.

Adult↗
PubMed1998

N-CPAP in the prevention of recurrent intubations and hospitalizations in a patient with refractory congestive heart failure.

A 61-year-old woman with ischemic cardiomyopathy continued to have recurrent episodes of respiratory failure secondary to acute pulmonary edema requiring ventilatory support on each occasion, despite undergoing surgical revascularization and mitral valve replacement. These episodes of acute respiratory failure were successfully averted by using nocturnal nasal continuous positive airway pressure (N-CPAP). Following N-CPAP, she was able to stay home for 207 consecutive days. Although well-designed, controlled studies are needed to validate this observation, nocturnal N-CPAP is a viable and cost effective option that may be considered in a select number of patients with end-stage cardiopulmonary disease.

Acute Disease↗
PubMed1994

Glomerular endothelial cell detachment in paired cadaver kidney transplants: evidence that some cadaver donors have pre-existing endothelial injury.

Poor initial function is common in cadaveric renal transplantation, and is usually attributed to acute tubular necrosis (ATN) brought about by ischemia during harvesting/implantation. However, this is often an assumption rather than a specific diagnosis. Recently, in 4 kidneys from 2 cadaver donors, we found evidence of severe endothelial injury, prior to exposure to cyclosporine or other known endothelial toxins. The biopsies at the time of completion of the transplant revealed apparent loss of glomerular endothelial cells on light microscopy, corresponding on electron microscopy to shrinkage of the endothelial cells away from the basement membranes of the capillary loops. Extensive microvascular thrombi were present. All 4 grafts displayed impaired initial function, which partially recovered with time. The finding of these unusual lesions in both kidneys from each of 2 donors suggested donor factors, although the only factor common to both donors was massive brain disruption. Thus, in the differential diagnosis of poor initial function in kidneys transplanted from cadaver donors, one should consider renal endothelial injury, which could lead to microthrombus formation, abnormal vasomotion, and functional impairment in the transplant.

Adult↗