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Biomedical subjects

G Eknoyan

Publications and source records attributed to G Eknoyan.

At least 73 records · Page 4Linked to original sources
PubMed1987

Structural and functional correlates of effects of angiotensin-induced changes in rat glomerulus.

The effects of systemically infused angiotensin II (ANG II) (5, 50, and 100 ng X min-1 X 100 g body wt-1; groups 1, 2, and 3, respectively) were studied in Sprague-Dawley rats. All doses increased systemic blood pressure, fractional excretion of sodium, and urine flow rate but decreased glomerular filtration rate. Scanning electron microscopy revealed no detectable changes in the visceral epithelium or measurable alterations in the total area of endothelial capillary surface occupied by pores. Glomerular basement membrane surface densities of outer (OCG) and inner (ICG) cortical glomeruli averaged 0.22 micron2/micron3 of glomerular tuft volume in all groups. Volume ratios of the individual glomerular tufts to that of their Bowman's capsule of OCG were less (P less than 0.05) in groups 1 and 2 (52 +/- 3 and 63 +/- 9%) than the control group (72 +/- 1%). The volume fraction of the glomerular capillaries to their Bowman's capsules remained approximately 25% in all groups. However, the volume fraction of parenchyma to Bowman's capsule was reduced in group 1 to 30 +/- 4% and 38 +/- 5% in group 2 compared with the control value of 47 +/- 2% (P less than 0.05). Thus ANG II reduced glomerular tuft volume and parenchyma but did not alter filtration surface area or capillary endothelial epithelial surface characteristics.

Angiotensin II↗
PubMed1986

Chronic renal failure. The primary care physician's role.

Recent developments in understanding of the pathophysiology of chronic renal failure have provided a sound basis for several measures which, when instituted early in the course of renal disease, can delay progression to end-stage kidney disease and considerably improved the symptoms of uremic syndrome. This article outlines the key role that the primary care physician plays in early diagnosis of chronic renal disease and institution of appropriate therapy well before the nephrologist's services are needed.

Absorption↗
PubMed1986

Determinants of plasma potassium levels in diabetic ketoacidosis.

The classic proposal of intracellular K+ for extracellular H+ exchange as responsible for the hyperkalemia of diabetic ketoacidosis (DKA) has been questioned because experimentally induced organic anion acidosis fails to produce hyperkalemia. It has been suggested, instead, that the elevated serum [K+] of DKA might be the result of the compromised renal function, secondary to volume depletion, that usually accompanies DKA. However, several metabolic derangements other than volume depletion and acidosis, which are known to alter potassium metabolism, also develop in DKA. This study of 142 admissions for DKA examines the possible role of alterations in plasma pH, bicarbonate, glucose (G), osmolality, blood urea nitrogen (BUN) and plasma anion gap (AG) on the levels of [K+]p on admission. Significant (p less than 0.01) correlations of [K+]p with each of these parameters were found that could individually account for 8 to 15 percent of the observed variance in the plasma potassium levels; however, the effects of some or all of these parameters on the [K+]p could be independent and therefore physiologically additive. Since the parameters under study are themselves interrelated, having statistically significant correlations with each other, their possible independent role on [K+]p was evaluated by multiple regression analysis. Only plasma pH, glucose and AG emerged as having a definite independent effect on [K+]p, with no independent role found for bicarbonate, BUN and osmolality. The equation that best describes [K+]p on admission for DKA was: [K+]p = 25.4 - 3.02 pH + 0.001 G + 0.028 AG, (r = 0.515). These results indicate that the endogenous ketoacidemia and hyperglycemia observed in DKA, which result primarily from insulin deficit, are the main determinants of increased [K+]p. Since exogenous ketoacidemia and hyperglycemia in the otherwise normal experimental animal do not increase [K+]p, it is postulated that insulin deficit itself may be the major initiating cause of the hyperkalemia that develops in DKA. Renal dysfunction by enhancing hyperglycemia and reducing potassium excretion also contributes to hyperkalemia.

Acid-Base Equilibrium↗
PubMed1986

Renal involvement in patients with thrombotic thrombocytopenic purpura.

A retrospective review of the records of 15 patients with thrombotic thrombocytopenic purpura (TTP) was performed to determine the spectrum of renal involvement that occurs in this disease. All cases exhibited some evidence of renal involvement, the most common manifestation of which was an abnormal urinalysis. Twelve cases (80%) had some degree of elevation of the serum urea nitrogen (SUN) or creatinine level at some time during the course of their disease. Renal involvement could be categorized into three types depending on the severity of TTP. In those cases presenting as an acute devastating illness, renal insufficiency, when present, was severe and a dominant component of the disease. In those that pursued a more protracted course, with subsequent acute exacerbations of TTP, renal insufficiency was variable and less severe than in the first group. In those presenting with a mild form of TTP, renal involvement consisted primarily of an abnormal urine sediment and azotemia that corrected rapidly following fluid replacement. A review of the literature beginning with 1966, when renal disease was established as part of the features that characterize TTP, provided 216 cases in whom sufficient data on renal involvement were recorded. Of the 168 cases where urinalysis was reported, hematuria was noted in 78% of the cases, proteinuria in 75, pyuria in 31, and cylindriuria in 24%. Of the 181 cases where the admission SUN was reported, it was higher than 20 mg/dl in 69% and greater than 60 mg/dl in 17% of the cases. The level of SUN was a significant determinant of the final prognosis of these patients.

Adolescent↗
PubMed1985

Microinjection study of renal calcium absorption in the phosphate-depleted rat.

Tracer microinjection studies were performed in chronically phosphate-depleted (CPD) and phosphate-supplemented (PS) rats in order to determine the site of the defect in calcium absorption which developed in CPD. Calcium recovery in the final urine was significantly higher in CPD than in PS rats after microinjections into the early and the late proximal tubules. However, there was no significant difference in the urinary recovery between the two groups after injection into the early and late distal convoluted tubules. The difference in calcium recovery in late proximal studies persisted during PTH infusion. This indicates that there is a defect in calcium absorption in phosphate-depleted rats between late proximal and early distal tubules, which is not correctable with PTH infusion.

Animals↗
PubMed1984

Effects of head-out water immersion on the urinary excretion of phosphate, calcium and magnesium in the awake dog.

The present study was undertaken to define the effects of heat-out water immersion on the urinary excretion of phosphate (UPO4V), calcium (UCaV), and magnesium (UMgV) in the awake dog. 53 dogs were divided into three groups: group I, time-control, from 10 a.m. to 4 p.m.; group II, immersion for 2 h, studied from 10 a.m. to 4 p.m., and group III, immersion for 2 h, studied from 4 p.m. to 10 p.m. Our results show that head-out water immersion did not alter the spontaneous pattern of UPO4V. When immersion was performed from 1 p.m. to 3. p.m. (group II), it had no effect on UCaV but induced a significant increase in UMgV although fractional excretion of Mg (FEMg) remained unchanged. When immersion was performed from 7 p.m. to 9 p.m. (group III), however, both UCaV and UMgV increased significantly. FECa also increased significantly in this group but FEMg again remained unchanged. The changes in UCaV were dissociated with UNaV. Changes in plasma PO4 (PPO4) and arterial pH were unrelated to changes in UCaV or UPO4V. Our findings show that head-out water immersion induces significant increases in UCaV and UMgV by mechanisms which are independent of parathyroid hormone (PTH) or acid base changes. The rise in UMgV seems to be related to an increase in the filtered load, while the increases in UCaV are secondary to changes in the renal tubular handling of calcium. Thus, under these experimental circumstances, Ca and Mg reabsorption seem to occur via different distal tubular pathways.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Endothelial characteristics of glomerular capillaries in normal, mercuric chloride-induced, and gentamicin-induced acute renal failure in the rat.

A reduction in glomerular capillary endothelial pore size and density has been reported in several models of acute renal failure. It has been suggested that these changes underlie the decrease in glomerular filtration rate and altered glomerular capillary hemodynamics measured in various experimental models of acute renal failure. We have thoroughly quantitated the surface characteristics of glomerular capillaries in control rats and in rats with either mercuric chloride-induced acute renal failure (2 mg/kg body wt) evaluated at 6 and 24 h after administration of the nephrotoxin or with gentamicin (G)1-induced acute renal failure evaluated after 8-9 d of 40 mg/kg body wt twice a day. Despite reductions in glomerular filtration rate in the experimental groups, no significant differences were observed between control (C) and any experimental group with respect to percent areas occupied by fenestrated endothelium (C = 53.6 +/- 2.7%; 6 h HgCl2 = 50.9 +/- 1.9%; 24 h HgCl2 = 53.9 +/- 5.7%; G = 56.7 +/- 2.4%), by cytoplasmic ridges (C = 31.2 +/- 1.5%; 6 h HgCl2 = 29.8 +/- 1.9%; 24 h HgCl2 = 30.6 +/- 3.1%; G = 26.5 +/- 1.5%), nonfenestrated endothelium (C = 15.5 +/- 4.0%; 6 h HgCl2 = 19.3 +/- 2.0%; 24 h HgCl2 = 15.6 +/- 4.3%; G = 16.9 +/- 2.3%), in the individual pore area expressed in square nanometers (C = 1,494 +/- 75; 6 h HgCl2 = 1,326 +/- 48; 24 h HgCl2 = 1,559 +/- 130; G = 1,340 +/- 101), or in the percentage of total pore area within fenestrated areas that were measured (C = 12.8 +/- 0.8%; 6 h HgCl2 = 11.2 +/- 0.7%; 24 h HgCl2 = 10.9 +/- 0.8%; G = 10.9 +/- 0.7%). These results provide quantitative data on the normal glomerular capillary endothelial surface characteristics and suggest that reductions of glomerular filtration rate in acute renal failure are not always associated with alterations in glomerular endothelial capillaries.

Acute Kidney Injury↗
PubMed1983

Protective effect of oral clonidine in the prophylaxis and therapy of mercuric chloride--induced acute renal failure in the rat.

Previous studies have demonstrated that the sympathomimetic agent clonidine, administered intravenously immediately prior to injury, provides partial protection against the acute structural and functional impairments associated with experimental ischemic and nephrotoxic ARF. To determine the effect of clonidine, administered orally, on the prolonged course of HgCl2-induced ARF, two groups of rats were studied for a period of 5 days after injury. For 5 days before HgCl2 administration (2 mg/kg s.c.) and throughout the study group I drank water while group II had clonidine (5 mg/L) added to water. The fatality rate was 77% in group I as compared to 11% in group II (p less than 0.001). Renal function (CCr and FENa) was better preserved and recovered more rapidly in group II rats protected with clonidine. Both groups showed varying degrees of proximal tubular cell injury, but group II had significantly fewer necrotic cells and demonstrated earlier evidence of regeneration. Whereas none of the injured cells in the clonidine-pretreated group revealed evidence of calcification, on the second day half the cells of the pars recta in the outer stripe of the medulla were calcified in group I. In group III animals, oral clonidine was started 2 hr after the injection of HgCl2 and also resulted in a significant reduction in fatality rate from 40% in control group to 0% in the clonidine-treated group. In addition, CCr and FENa were better preserved and recovered more rapidly in this group of clonidine-treated rats. These results indicate that oral clonidine, administered either before or shortly after HgCl2-induced ARF, exerts a salutory effect on the course and mortality of ARF by providing protection of renal function and enhancement of the recovery process.

Acute Kidney Injury↗
PubMed1982

Plasma acid-base patterns in diabetic ketoacidosis.

In a study of the types of plasma acid-base patterns present at 196 admissions for diabetic ketoacidosis we found no relation between the initial level of serum total carbon dioxide and the plasma anion gap; instead, there was a broad spectrum of acid-base patterns, ranging from pure anion-gap acidosis to pure hyperchloremic acidosis. Although the degree of renal dysfunction on admission, which reflected the magnitude of volume depletion, was independent of the severity of metabolic acidosis, it was responsible for the variable retention of plasma ketones: the more severe the volume depletion on admission, the greater the ketone retention and the less prominent the hyperchloremic acidosis. Recovery from acidosis was significantly slower in patients admitted with pure hyperchloremic acidosis. After therapy, hyperchloremia developed in most patients at four to eight hours after admission, because of the retention of chloride in excess of sodium and the excretion of ketones by the kidney.

Acid-Base Equilibrium↗
PubMed1982

Renal papillary necrosis: an update.

The clinical and diagnostic features of renal papillary necrosis (RPN) of 27 patients were studied. Diabetes mellitus was the most frequent (56%) condition associated with RPN. Analgesic abuse, sickle hemoglobinopathy and urinary tract obstruction were present in 4 patients each; in 6 of these 12 patients these conditions were present as a coexistent disease with diabetes mellitus. There was evidence of an acute or chronic infection of the urinary tract in 18 patients, as a coexistent condition with another underlying disease that itself can cause RPN in 14 patients and as the only cause of RPN in another 4. Thus, the presence of more than one diagnostic condition which might be implicated in the causation of RPN was present in 15 patients or 55% of the cases in this series. When infection was excluded, six patients or 22% of the cases had two coexisting diseases, each of which has been implicated as a cause of RPN. This observation underlines the multifactorial nature of this entity and might explain why RPN is not encountered more frequently in each of the various primary diseases with which it has been associated. The average age of the patients at the time of diagnosis was 53 years for women and 56 years for men. Only six of the patients were younger than 40 years, and three of these had sickle hemoglobinopathy. The diagnosis of RPN was based on x-ray findings in eight patients, on the histologic examination of papillary tissue in urine in one, and on autopsy findings in the rest. Papillary necrosis was bilateral in three-fourths of the cases. The clinical picture varied. Most of the patients (67%) presented with chills and fever. Flank pain and dysuria were present in 11 patients (41%). As a rule oliguria was rare and progressive uremia was uncommon. In cases diagnosed at post-mortem, the patients had succumbed to infection or to a primary severe extrarenal disorder with the possibility of RPN having been entertained clinically in only half these cases prior to autopsy.

Adolescent↗
PubMed1982

Phosphate therapy in diabetic ketoacidosis.

To determine the efficacy of phosphate replacement in the therapy for diabetic ketoacidosis (DKA), 44 patients were randomly assigned to three treatment groups: those who received no phosphate replacement, those who received 15 mmole of sodium phosphate at the fourth hour, or those who received 15 mmole of sodium phosphate at 2, 6, and 10 hours. All patients were treated with intravenous insulin injection (0.1 units/kg/hr), fluids, and potassium. Four hours after a 15-mmole sodium phosphate infusion, the serum phosphate level was 2.8 +/- 0.8 mg/dL vs 2.1 +/- 0.8 mg/dL in the control patients; however, this dose was insufficient to maintain the serum phosphate level at 16 and 24 hours. Forty-five millimoles of phosphate prevented severe hypophosphatemia in all but one patient and produced substantially higher phosphate levels at 8, 16, and 24 hours. Phosphate therapy did not affect the duration of DKA, dose of insulin required to correct the acidosis, abnormal muscle enzyme levels, glucose disappearance, or morbidity and mortality. Although theoretically appealing, phosphate therapy is not an essential part of the therapy for DKA in most patients.

Adolescent↗