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Biomedical subjects

S A Mazbar

Publications and source records attributed to S A Mazbar.

7 recordsLinked to original sources
PubMed2001

Emergency laparotomy in patients on continuous ambulatory peritoneal dialysis.

Peritonitis is the most common complication of chronic ambulatory peritoneal dialysis (CAPD). It is often a diagnostic challenge to differentiate those patients with CAPD-associated infections from those who have unrelated gastrointestinal pathology as the cause of peritonitis and would benefit from surgical exploration. A retrospective chart review was performed on all patients at a single institution who were on CAPD between the years 1990 and 1998 and who underwent laparotomy for peritonitis. Six patients underwent laparotomy. Four were male and two were female; ages ranged from 34 to 80 years. Perforated appendicitis was the cause of peritonitis in three patients, perforated diverticulitis was present in two, and one was without any suppurative intra-abdominal process. In each case CT scan of the abdomen was nondiagnostic. There was a delay in diagnosis of 10 days (range 3-21 days) and an operative mortality of 16 per cent.

Adult↗
PubMed1997

Long-term captopril treatment restores natriuresis after carotid baroreceptor activation in the SHR.

In anesthetized Sprague-Dawley rats, intermittent bilateral carotid artery traction (BilCAT) caused a transient decrease in mean arterial pressure (MAP) of 28 +/- 3 mmHg and led to a progressive increase in sodium excretion (UNaV) that nearly doubled 45-90 min after initiation of the repetitive application of BilCAT (P < 0.001). This natriuresis was accompanied by an increase in glomerular filtration rate (GFR) from 2.70 +/- 0.3 to 3.2 +/- 0.3 ml/min (P < 0.001), no change in renal plasma flow [clearance of p-aminohippurate (PAH)], and an increase in the fractional excretion of lithium. Rats with bilateral renal denervation exhibited neither natriuresis nor an increase in GFR in response to BilCAT despite similar vasodepression caused by the maneuver. Normotensive Wistar-Kyoto (WKY) rats responded to BilCAT like Sprague-Dawley rats, whereas spontaneously hypertensive rats (SHR) exhibited an exaggerated vasodepressor response to BilCAT (-51 +/- 3 mmHg) without increasing either UNaV or GFR. Separate groups of WKY and SHR were treated from 4 wk of age with captopril added to the drinking water at a concentration of 1 g/l. At 12-14 wk, both groups had lower MAP compared with untreated animals. Captopril treatment did not alter either the natriuretic response or the increase in GFR seen in untreated WKY after BilCAT, and the maneuver produced equivalent degrees of vasodepression as in controls. However, treated SHR now responded to BilCAT with increases in both UNaV and GFR that closely resembled the responses seen in Sprague-Dawley and WKY rats. These results suggest that BilCAT produces natriuresis through a pathway dependent on the renal nerves. This pathway does not function in untreated SHR despite similar vasodepression. Long-term treatment with captopril restores this reflex pathway in SHR, lending support to the concept that angiotensin II is critically linked to heightened sympathetic nerve activity and abnormal sodium metabolism in this strain.

Analysis of Variance↗
PubMed1996

Rolaids-yogurt syndrome: a 1990s version of milk-alkali syndrome.

Milk-alkali syndrome is characterized by progressive hypercalcemia, systemic alkalosis, and renal insufficiency. After calcium carbonate is ingested with diary products, hypercalcemia and alkalosis may develop in susceptible persons, particularly those with underlying renal insufficiency. We describe a young woman who neither drank milk nor had peptic ulcer disease, yet who ingested enough calcium carbonate to require admission to an intensive care unit for acute renal failure. Chronically bulimic, she was taking Rolaids (Warner-Lambert Co, Morris Plains, NJ), which contained calcium carbonate, and was eating yogurt daily to prevent osteoporosis. We discuss the characteristics and complex metabolic interactions of the milk-alkali syndrome, a critical but generally reversible electrolyte disorder. Early recognition of coincident hypercalcemia and alkalosis and prompt cessation of calcium carbonate ingestion are essential for successful recovery. Finally, we suggest that nephrologists should discourage patients with renal insufficiency and chronic vomiting from consuming calcium-containing antacids and excessive dietary calcium.

Acute Kidney Injury↗
PubMed1990

Renal involvement in patients infected with HIV: experience at San Francisco General Hospital.

A spectrum of renal abnormalities has been described in patients infected with the human immunodeficiency virus (HIV) with or without signs of the acquired immunodeficiency syndrome (AIDS). In particular, attention has been focused on a nephropathy characterized clinically by nephrotic proteinuria and rapidly advancing renal insufficiency, and histologically by focal and segmental glomerulosclerosis (FSGS). To evaluate the relationship between HIV infection and structural renal disease, we reviewed all consultations between January 1982 and March 1988 to the Division of Nephrology at San Francisco General Hospital (SFGH), a municipal hospital treating approximately one-third of AIDS cases in San Francisco. Seventy-three consultation requests were received during this period regarding patients with AIDS (48), AIDS-Related Complex (23), or asymptomatic HIV infection (2). Of these, 27 gave evidence of structural renal disease (Group I): 14 had chronic renal insufficiency, in 10 of whom nephrotic proteinuria was also present. However, progression of renal insufficiency to end-stage renal disease (ESRD) in this group did not follow the rapid course described for HIV-associated nephropathy. Renal tissue was examined in 11 Group I patients and showed FSGS in four and a variety of acute and chronic glomerular and tubulointerstitial changes in the others. In 46 Group II patients, consultation was requested for acute renal failure or fluid, electrolyte, and acid-base disturbances. We also reviewed 91 consecutive autopsies performed in patients dying with AIDS at SFGH between 1981 and 1986.(ABSTRACT TRUNCATED AT 250 WORDS)

AIDS-Related Complex↗
PubMed1990

Mechanism of the natriuretic effect of unilateral carotid artery traction in the rat.

Unilateral traction on a carotid artery is known to activate the carotid baroreceptor reflex. This maneuver increases sodium excretion in a manner not completely dependent on the renal nerves, suggesting that a humoral factor(s) could be involved. We measured sodium excretion before and after unilateral carotid artery traction or sham traction in anesthetized rats and related the results to the plasma concentration of immunoreactive (IR)-gamma-melanocyte stimulating hormone (gamma-MSH), a peptide known to be natriuretic in other circumstances. In 12 rats undergoing sham traction, sodium excretion did not change and plasma IR-gamma-MSH activity at the end of the experiment was 10.5 +/- 5.4 (SD) fmol/mL. Carotid artery fraction in 20 other rats caused a transient dip in mean arterial pressure of 20.1 +/- 13.2 mm Hg, and sodium excretion increased from 746 +/- 431 to 1,739 +/- 1,436 nEq/min (P less than 0.005). Plasma IR-gamma-MSH was increased to 21.1 +/- 7.1 fmol/mL (P less than 0.001 versus sham). Prior ipsilateral carotid sinus denervation markedly attenuated the carotid artery traction-related dip in blood pressure and prevented both the natriuresis and the increase in IR-gamma-MSH activity seen after this maneuver in intact rats. Pretreatment with anti-gamma-MSH antiserum also blocked the natriuretic response to carotid artery traction, despite a similar transient dip in blood pressure of 18.3 +/- 9.9 mm Hg. These observations suggest that activation of the carotid baroreceptor reflex by unilateral carotid artery traction causes natriuresis that is mediated largely by an increase in the plasma concentration of a peptide or peptides closely related to the gamma-MSH sequence.

Animals↗