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Biomedical subjects

W L Henrich

Publications and source records attributed to W L Henrich.

At least 37 records · Page 2Linked to original sources
PubMed1997

Anemia, hypertension, and myocardial dysfunction in end-stage renal disease.

Cardiovascular disease remains the major cause of mortality in patients with end stage renal disease (ESRD). The pathophysiology of cardiac dysfunction in ESRD is complex and not fully understood. However, it appears that the two major determinants of left ventricular (LV) hypertrophy and dysfunction are anemia and hypertension, both of which are very common in ESRD patients. Early and aggressive correction of anemia and hypertension may have a significant impact on cardiac disease in ESRD patients. This article presents a discussion on the management of anemia and hypertension, and the current information available on the pathogenesis and management of LV dysfunction in ESRD.

Anemia↗
PubMed1996

The renal effects of nonsteroidal anti-inflammatory drugs: summary and recommendations.

The renal effects of nonsteroidal anti-inflammatory drugs are reviewed with special emphasis on the clinical, pathophysiologic, and risk factors for acute renal failure. Renal papillary necrosis and chronic renal insufficiency can occur with the prolonged use of these drugs, although the prevalence of this manifestation of nonsteroidal anti-inflammatory drug nephrotoxicity is unknown. Current recommendations based on a critical literature survey are provided, along with a list of suggested areas in which more research is needed.

Acute Kidney Injury↗
PubMed1996

Differential regulation of rat glomerular and proximal tubular renin mRNA following uninephrectomy.

Angiotensin II is thought to play a role in the renal adaptations to reduced renal mass, but earlier work has shown that plasma renin activity (PRA) does not increase in this setting. To examine this paradox, we studied the effect of uninephrectomy (UNX) on circulating, juxtaglomerular, glomerular, and proximal tubular (PT) renin. PRA was unchanged 2 wk following UNX and fell slightly at 6 wk. Single kidney renin secretory capacity and cortical renin mRNA, reflecting juxtaglomerular renin, were unchanged at 2 and 6 wk. With quantitative competitive reverse transcription-polymerase chain reaction, renin mRNA in microdissected glomeruli and PT were dramatically increased 2 wk post-UNIX (for glomeruli: sham, 1.2 +/- 0.3, vs. UNX, 8.8 +/- 1.9 x 10(5) copies/glomerulus; for PT: sham, 4.6 +/- 0.9, vs. UNX, 17.7 +/- 5.1 x 10(3) copies/mm). By 6 wk, glomerular renin was unchanged, and PT renin mRNA was markedly suppressed (for glomeruli; sham, 2.9 +/- 1.2, vs. UNX, 4.2 +/- 1.1 x 10(5) copies/glomerulus; for PT: sham, 7.5 +/- 2.1, vs. UNX, 1.0 +/- 0.3 x 10(3) copies/mm). These results demonstrate differential regulation of the circulating, juxtaglomerular, glomerular, and PT renin systems. Early activation of glomerular and PT renin may result in increased local generation of angiotensin II and thereby affect renal structural and functional adaptations following UNX.

Animals↗
PubMed1996

Renin regulation in cultured proximal tubular cells.

Recent studies have documented the presence of a complete renin-angiotensin system in the proximal tubule of the kidney: however, little is known about the regulation of renin in this proximal tubular system. Therefore, we performed the present studies to learn whether the behavior of the renin system in cultured proximal tubule is similar to that of the juxtaglomerular renin system. Basal renin secretion from rabbit proximal tubular cells in primary culture was low and not affected by isoproterenol (10(-5) mol/L), diltiazem (10(-5) mol/L), or a zero-calcium bath (O nmol/L). Only the calcium ionophore A23187 (10(-4) mol/L) significantly reduced renin secretion in these cells (from 2.44 +/- 0.37 to 1.14 +/- O.08 ng angiotensin I/mg protein per hour, P<.05). When the proximal tubular cells were lysed so the effects of the test agents on intracellular renin content could be assessed, isoproterenol caused a significant twofold (107 percent) increase (from 2.02 +/- 0.56 to 4.18 +/- 0.81 ng angiotensin I/mg protein per hour, P<.05), whereas diltiazem, A23187, and zero- and high-calcium baths did not produce a significant change. The effects of these agents on renin mRNA were examined in rabbit and rat proximal tubular cells in primary culture with the use of an S1 nuclease protection assay. Densitometry analysis of renin mRNA and either GAPDH mRNA (rat) or alpha-actin (rabbit) showed no significant alterations in renin mRNA abundance. In summary, these results confirm the presence of renin mRNA in cultured proximal tubular cells and suggest that a low-level, constitutive secretion of renin occurs in this system that is decreased by A23187. Moreover, the results also suggest that proximal tubular renin is regulated, albeit differently from the juxtaglomerular renin system. Finally, short-term increments in proximal tubular renin occur without a change in renin mRNA.

Animals↗
PubMed1996

Distal vessel atherosclerosis as a cause for false-positive renal scintigraphy.

While captopril-enhanced renal scintigraphy is acknowledged to be a useful screening technique to detect clinically silent obstructive lesions of the main renal arteries, the presence of significant atherosclerosis of distal, smaller renal vessels as a cause of positive scintigraphy scans has not been reported extensively. In a retrospective 2-year analysis of 31 consecutive captopril-enhanced renal scintigrams, we found a total of 13 studies in 11 patients that were classified as "positive" for renal artery stenosis. Of these 11 patients with positive scintigraphic studies, 4 patients underwent 5 renal arteriography procedures; only 1 of these renal arteriograms showed significant stenosis of the main renal artery. In the other 4 cases, an angiographic pattern of diffuse intrarenal distal arterial disease correlated with scintigram lateralization. Angiography was also performed in 4 patients with negative captopril renal scintiscans. In each of these cases the arteriogram was also negative for significant renal artery stenosis, and only 1 patient had diffuse bilateral intrarenal arterial disease. We conclude that distal renal arterial narrowing should be considered in the differential diagnosis of lateralized renal scintigrams. A negative renal scintigraphic study may be more reliable for excluding significant main renal artery obstructive disease.

Adult↗
PubMed1995

In vitro production of angiotensin II by isolated glomeruli.

The glomerulus has several components of the renin-angiotensin system (RAS). The purpose of this study was to evaluate the ability of glomeruli isolated from adult Wistar-Kyoto rats to produce angiotensin II (ANG II). When isolated glomeruli were incubated in Krebs buffer, the peak concentration of immunoreactive angiotensin (ANG) in the incubation medium, representing simultaneous production and degradation, occurred after 15 min of incubation (3.98 +/- 0.34 pg.mg protein-1.15 min-1, of which 18% was ANG II. When 125I-labeled ANG II was incubated with isolated glomeruli, the half-life of ANG II was 6.06 min. Hence, we estimated ANG II production at 3.77 +/- 0.21 pg.mg protein-1.15 min-1. When angiotensinogen-rich serum was added to the incubation medium, ANG concentration at 15 min increased by 500-fold (1,978 +/- 44 pg.mg protein-1.15 min-1, P < 0.001). ANG concentration in the glomerular incubate responded to perturbations known to alter systemic RAS. Enalaprilat, chymostatin, propranolol, and renin antiserum decreased ANG concentration in glomerular incubate, whereas salt depletion increased this (P < 0.05). We conclude that the rat glomerulus can generate ANG II independent of neural, hormonal, or vascular control.

Angiotensin II↗
PubMed1995

Pharmacokinetics of fluconazole in renal failure.

Fluconazole (FLU) is a widely used antifungal agent. The multiple-dose pharmacokinetics of FLU in renal impairment have not been previously investigated. The following groups were studied: volunteers with creatinine clearances (CLcr, > 50 mL/min) of 107 mL/min, given a loading dose of 400 mg and a daily dose of 200 mg/day for 9 days (Group 1); subjects with CLcr between 21 and 50 mL/min with a mean of 38 mL/min, given a loading dose of 200 mg and a maintenance dose of 100 mg/day for 9 days (Group 2); subjects with CLcr between 11 and 20 mL/min with a mean of 14.8 ml/min, given a loading dose of 100 mg and a maintenance dose of 50 mg/day for 9 days (Group 3); and subjects on hemodialysis (three times per week) receiving a loading dose of 200 mg and then 100 mg after each of four dialysis sessions (Group 4) (N = 10 per group). After the administration of the loading dose on Day 1, the mean area under the curve (AUC) (0-24) measurements were approximately proportional to the dose of FLU and independent of renal function. After 10 days of FLU dosing, the mean renal clearance of FLU decreased as CLcr decreased for Groups 1 to 3, and the Day 10 mean half-lives were inversely related to mean CLcr (36.7 h in Group 1, 84.5 h in Group 2, and 101.9 h in Group 3). The mean AUC (0-24) on Day 10 was similar for Group 1 compared with Group 2, despite a reduction in the maintenance dose by 50%. (ABSTRACT TRUNCATED AT 250 WORDS)

Creatinine↗
PubMed1995

Systemic mucormycosis complicating acute renal failure: case report and review of the literature.

Mucormycoses is a fungus which increasingly has been reported as a cause of opportunistic infection during the last 40 years. This infection is most commonly associated with underlying predisposing conditions, particularly diabetic ketoacidosis, hematologic and other malignancies, steroid therapy, broad-spectrum antibiotic therapy, or various acquired and hereditary immunodeficient disease states. The present report is that of a previously healthy patient with acute renal failure secondary to a postviral rhabdomyolysis syndrome, who received corticosteroids and developed unsuspected and undiagnosed systemic mucormycosis. Autopsy revealed that he died as a consequence of a massive pulmonary hemorrhage due to disseminated invasive mucormycosis, involving both the lungs and kidneys. A review of the literature reporting disseminated mucormycosis in association with renal failure is provided. Mucormycosis should be considered in immunocompromised patients with renal failure and fevers of unknown origin so that early diagnosis and prompt surgical and medical therapy may be instituted.

Acute Kidney Injury↗
PubMed1995

Clinical acute renal failure with nonsteroidal anti-inflammatory drugs.

Under baseline euvolemic conditions, prostaglandins play little to no role in the minute-to-minute regulation of renal function. Where these compounds come to serve a major role is in the setting of a systemic or intrarenal circulatory disturbance. In the setting of a decreased absolute or effective circulatory volume, a number of vasoconstrictor effectors are stimulated whose function is to preserve the systemic circulation. At the same time, these compounds stimulate the synthesis of renal vasodilatory prostaglandins. In turn, prostaglandins oppose the vasoconstrictive effect of these effectors such that the renal circulation remains well-preserved while the rest of the circulation is clamped down. Predictably, inhibition of prostaglandin synthesis would lead to unopposed renal vasoconstriction, resulting in a precipitous decline in renal function. Clinical conditions in which the renal circulation is critically dependent on the effect of vasodilatory prostaglandins include volume depletion, congestive heart failure, and cirrhosis. There are other conditions in which the circulatory volume is normal, but due to the intrarenal generation of vasoconstrictors, the kidney is similarly dependent on vasodilatory prostaglandins. Such conditions include glomerulonephritis and urinary tract obstruction.

Acute Kidney Injury↗
PubMed1994

Nephrotoxicity of nonsteroidal anti-inflammatory drugs.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are important therapeutic agents in the management of rheumatologic disorders and other pain syndromes. Over the counter availability of the drugs has expanded the usage of the drugs. This article reviews the nephrotoxicity of these drugs, with some emphasis on NSAID-related proteinuria. Although reversibility of renal involvement upon drug discontinuance is the rule, progression to end-stage renal disease has occurred. A proposed guideline for monitoring renal impairment in low- and high-risk patients is also presented.

Acute Kidney Injury↗
PubMed1993

Effects of cooler temperature dialysate on hemodynamic stability in "problem" dialysis patients.

Symptomatic hypotension is a common and disabling complication of hemodialysis treatments. The incidence of symptomatic hypotensive episodes is particularly high in patients who have normal or low blood pressure at the initiation of dialysis and in patients who have large interdialytic weight gains. The aim of this study was to determine whether cooling the dialysate temperature from 37 degrees C to 35 degrees C improved tolerance to dialysis in a group of 12 of these "problem" patients. A double-blinded protocol was performed in six hypotension-prone and six large weight gainers who were subjected to two identical hemodialyses except for the dialysate temperature of 37 degrees C or 35 degrees C. Changes in biochemical parameters and weight were comparable during the two maneuvers. Recumbent blood pressure declined significantly (P < 0.01) during 37 degrees C dialysis but not 35 degrees C dialysis; blood pressure was significantly lower at 1, 2, and 3 hours of 37 degrees C dialysis compared to 35 degrees C dialysis (P < 0.05). Further, both supine and upright blood pressure was significantly lower following 37 degrees C dialysis (P < 0.02). This lower blood pressure was present in both subgroups of patients. All 18 episodes of symptomatic hypotension noted during the study occurred during 37 degrees C dialysis. A significantly greater increase in peripheral vascular resistance (calf blood flow was measured directly by venous occlusion plethysmography) occurred upon exposure to the 35 degrees C dialysate in both subgroups of patients (P < 0.01); supine and upright post-dialysis plasma norepinephrine values were also significantly greater (P < 0.001) after 35 degrees dialysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Renin expression in renal proximal tubule.

Angiotensinogen, angiotensin-converting enzyme, and renin constitute the components of the renin-angiotensin system. The mammalian renal proximal tubule contains angiotensinogen, angiotensin-converting enzyme, and angiotensin receptors. Previous immunohistochemical studies describing the presence of renin in the proximal tubule could not distinguish synthesized renin from renin trapped from the glomerular filtrate. In the present study, we examined the presence of renin activity and mRNA in rabbit proximal tubule cells in primary culture and renin mRNA in microdissected proximal tubules. Renin activity was present in lysates of proximal tubule cells in primary culture. Cellular renin content in cultured proximal tubule cells was increased by incubation with 10(-5) M isoproterenol and 10(-5) M forskolin by 150 and 110%, respectively. In addition, renin transcripts were detected in poly(A)+ RNA from cultured proximal tubule cells by RNA blots under high stringency conditions. In microdissected tubules from normal rats, renin mRNA was not detectable with reverse transcription and polymerase chain reaction. However, in tubules from rats administered the angiotensinogen-converting-enzyme inhibitor, enalapril, renin was easily detected in the S2 segment of the proximal tubule. We postulate the existence of a local renin-angiotensin system that enables the proximal tubule to generate angiotensin II, thereby providing an autocrine system that could locally modulate NaHCO3 and NaCl absorption.

Animals↗
PubMed1993

The renal proximal tubule renin-angiotensin system.

In conclusion, a complete RAS is present in the mammalian proximal tubule that is potentially autocrine and paracrine in nature. Maneuvers that stimulate renin in JG cells and renal vasculature appear to also stimulate renin in the proximal tubule. The subcellular localization of the different components and the regulation of this epithelial RAS still remain to be defined. This RAS may be important in regulation of proximal tubule NaCl and NaHCO3 transport. Finally, one can speculate that activation of this RAS may play a pathogenetic role in some patients with essential hypertension and in the hypertension and cyst growth seen in autosomal dominant polycystic kidney disease.

Animals↗
PubMed1992

Improved left ventricular contractility with cool temperature hemodialysis.

Cool temperature dialysis (CTD) has been shown to sharply decrease the frequency of intradialytic hemodialysis hypotension, but the mechanism of this hemodynamic protection is unknown. Therefore, we performed two-dimensional echocardiographic studies of left ventricular contractility in six stable hemodialysis patients before and after hemodialysis at 37 degrees C (RTD) and 35 degrees C (CTD). Left ventricular function was assessed by plotting the rate-corrected velocity of circumferential fiber shortening (Vcfc) against end-systolic wall stress (sigma es) at four different levels of afterload. Linear regression was used to calculate Vcfc at a common afterload of 50 g/cm2. Changes in weight and dialysis parameters were similar following RTD and CTD. Mean arterial pressure and heart rate did not change significantly following RTD or CTD. The Vcfc - sigma es relation was shifted upward in each patient after CTD, indicating increased contractility as compared to RTD or pre-dialysis baseline. Pre-dialysis Vcfc at an afterload of 50 g/cm2 was similar during RTD and CTD (0.94 +/- 0.24 circ/sec vs. 0.92 +/- 0.22 circ/sec). Postdialysis Vcfc at an afterload of 50 g/cm2 was significantly higher for CTD than for RTD (1.13 +/- 0.29 circ/sec vs. 0.98 +/- 0.30 circ/sec, P = 0.0004). Thus, cool temperature dialysis increases left ventricular contractility in hemodialysis patients, which may be a potential mechanism whereby hemodynamic tolerance to the dialysis procedure is improved.

Adult↗
PubMed1992

Inhibition of renin secretion from rat renal cortical slices by (R)-12-HETE.

The arachidonic acid metabolite 12-hydroxyeicosatetraenoic acid (12-HETE) inhibits renin secretion both in vivo and in vitro, but the enzymatic origin of the 12-HETE responsible for renin inhibition is unknown. These studies examined the effect of the 12-HETE stereoisomers (R)-12-HETE (a product of the cytochrome P-450 monooxygenase enzyme system) and (S)-12-HETE (a product of the lipoxygenase enzyme system) on basal and stimulated renin secretion from superficial cortical slices in the rat. First, rat cortex was shown to produce 12-HETE; chiral-phase high-performance liquid chromatography revealed that cortex produced 81% (S)-12-HETE and 19% (R)-12-HETE. (R)-12-HETE reduced basal renin release by 28 +/- 4% to 49 +/- 5% at concentrations of 10(-9) to 10(-7) M (P < 0.05 to 0.01). (S)-12-HETE did not significantly affect renin release. (R)-12-HETE also blunted isoproterenol-stimulated renin secretion (P < 0.05) at a concentration of 10(-6) M. 20-HETE, another cytochrome P-450 product, did not exert a significant effect on renin release. In summary, both (R)-12-HETE and (S)-12-HETE are synthesized by renal cortical tissue. Only (R)-12-HETE directly inhibits in vitro renin release. These findings suggest that the renal cytochrome P-450 enzyme system is capable of directly influencing local renin secretion.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1991

The endothelium--a key regulator of vascular tone.

Emerging evidence suggests the endothelium produces several substances capable of locally regulating organ blood flow. Vasoactive prostaglandins, endothelium-derived relaxing factor, and endothelin are examples of these vasoactive substances. Abnormalities of endothelial function may contribute to the pathogenesis of disease in several circumstances, including hypertension, diabetes, and septicemia. Evidence for the endothelium as a regulator of regional perfusion and several of the endothelium-derived substances and their potential role in disease are reviewed.

Aging↗