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J R Diamond

Publications and source records attributed to J R Diamond.

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

Ameliorative effects of dietary protein restriction in chronic aminonucleoside nephrosis.

Because many investigators have demonstrated the efficacy of dietary protein restriction in various experimental models of glomerular injury that progress to focal and segmental glomerulosclerosis (FSGS), we used this dietary maneuver in chronic aminonucleoside nephrosis. This model of glomerular disease, which uses a single intravenous injection of the puromycin aminonucleoside (PAN), slowly progresses over 18 weeks with mesangial cell proliferation and FSGS as the pathologic hallmarks. We performed renal functional and histopathologic studies in 21 rats with chronic aminonucleoside nephrosis. Group 1 rats (n = 10) were fed a standard rodent diet containing 23.4% protein, whereas group 2 animals (n = 11) were maintained with a 6% protein diet replete with electrolytes, minerals, and vitamins. In those animals subjected to dietary protein restriction, proteinuria was significantly reduced at 14, 28, 84, and 126 days after PAN administration. In rats maintained with the 6% protein diet at 126 days after PAN delivery, there was also a significant reduction in the percent of glomeruli with segmental areas of glomerulosclerosis or hyalinosis and mesangial cell proliferation. We conclude that the renal functional and histologic consequences of chronic aminonucleoside nephrosis can be blunted by dietary protein restriction.

Animals↗
PubMed1986

A role for oxygen free radicals in aminonucleoside nephrosis.

The cellular processes responsible for the proteinuria induced by the aminonucleoside of puromycin (PA) remain inadequately defined. Hypoxanthine is both a metabolic breakdown product of PA as well as a substrate for xanthine oxidase, which catalyzes its enzymatic conversion to xanthine and uric acid, yielding the superoxide anion in the process. We examined whether oxygen free radical production contributes to the development of proteinuria in this model. Seven groups of male Sprague-Dawley rats were studied. Proteinuria was quantitated and histology examined 7 days after rats were treated with PA intravenously over 5 min. PA-treated animals received either saline, dimethyl sulfoxide, superoxide dismutase, or catalase over 30 min prior to and 30 min following PA administration. Another group received allopurinol over 4 hr prior to PA. The superoxide dismutase and allopurinol treatment groups had a significant suppression of urinary protein excretion compared to the PA control group. There were also less severe glomerular morphologic changes in the superoxide dismutase group vs. the PA controls, which demonstrated a pathologic pattern that included epithelial cell blebbing, segmental mesangial cell proliferation and matrix expansion, loss of glomerular capillary lumina, and occasional adhesions between the glomerular tuft and Bowman's capsule. The allopurinol group exhibited normal glomerular morphology on light microscopy, with the exception of occasional epithelial cell blebs. All groups showed spreading of the epithelial cell cytoplasm along the glomerular basement membrane with loss of foot processes, focal areas of lifting of the epithelial cell from the glomerular basement membrane, cytoplasmic vacuolization, and protein reabsorption droplets; however, allopurinol-treated animals demonstrated these changes to a lesser extent.(ABSTRACT TRUNCATED AT 250 WORDS)

Allopurinol↗
PubMed1986

Nonanticoagulant protective effect of heparin in chronic aminonucleoside nephrosis.

Aminonucleoside nephrosis progresses over an 18-week period to focal and segmental glomerulosclerosis (FSGS). Whole heparin has been shown to blunt the extent of renal injury in another model of FSGS, renal ablation; however, the precise mechanism of protection has remained uncertain. Since heparin has a variety of physiologic actions unrelated to anticoagulation, we administered three different heparin compounds, each with a distinct profile of biological properties, to groups of rats given a single intravenous dose of puromycin aminonucleoside (PA). In the absence of a prolongation of the activated partial thromboplastin time (aPTT), both whole heparin (WH) and a 7,000- to 11,000-dalton-molecular-weight nonanticoagulant heparin (NAH) ameliorated the functional and histologic abnormalities of chronic aminonucleoside nephrosis as evidenced by significant reductions in 24-hour urine protein excretion while preserving the glomerular filtration rate and blunting the rise in serum creatinine as compared to untreated PA control animals at the conclusion of the study. In addition, the NAH and WH groups exhibited significantly fewer glomeruli with either segmental mesangial proliferative areas or glomerulosclerosis/hyalinosis lesions 18 weeks after PA administration. A fragment of heparin (HF) was ineffective. We conclude that heparin may exert its beneficial effect in chronic aminonucleoside nephrosis through a biologic action, other than anticoagulation, perhaps by inhibition of mesangial cell proliferation.

Animals↗
PubMed1986

Focal and segmental glomerulosclerosis following a single intravenous dose of puromycin aminonucleoside.

Focal and segmental glomerulosclerosis (FSGS) represents a final pathologic pattern of a number of human renal disorders. Among laboratory models, repeated intraperitoneal injections of the aminonucleoside of puromycin (PA) produces a histologic pattern not unlike the human process. A single intravenous dose of this drug usually results in glomerular morphologic changes in rats resembling those in human nephrotic syndrome with minimal changes. This report describes acute and chronic glomerular injury that begins as early as 8 days after a single central administration of PA and progresses to FSGS within an 18-week period. It seems likely that minimal change disease and FSGS are two pathologic processes in the same continuum of disease. In this model, the severity and persistence of the glomerular lesion may represent irreversible glomerular epithelial cell (GEC) injury secondary to the toxic effects of PA.

Animals↗
PubMed1985

Fractional excretion of sodium. Exceptions to its diagnostic value.

Determining the cause of acutely deteriorating renal function is a common problem in clinical nephrology. The fractional excretion of filtered sodium (FENa) has been demonstrated to be a reliably discriminating test between prerenal azotemia and acute tubular necrosis. However, with increasing clinical use of the FENa, numerous reports of low FENa (less than 1%) have appeared. The clinical settings of these reports include oliguric and nonoliguric acute tubular necrosis, urinary tract obstruction, acute glomerulonephritis, hepatorenal syndrome, renal allograft rejection, sepsis, and drug-related alterations in renal hemodynamics. One particular urinary index cannot be expected to reliably discriminate between prerenal azotemia and acute renal failure in all cases. The utility of the FENa test in the differential diagnosis of acute renal failure must be interpreted in conjunction with the patient's clinical course and the use of additional urinary and serum tests.

Acute Kidney Injury↗
PubMed1984

Nifedipine-induced renal dysfunction. Alterations in renal hemodynamics.

Nifedipine caused acute, reversible deterioration in renal function in four patients with chronic renal insufficiency. The absence of hypotension, clinical course, benign urinary sediments, and normal results of renal ultrasound examinations excluded acute tubular necrosis, pyelonephritis, interstitial nephritis, obstructive uropathy, and acute glomerulonephritis. It is postulated that this slow calcium channel blocker produced deleterious intrarenal hemodynamic alterations in the setting of moderate to severe renal functional impairment. Nifedipine may alter renal function by blocking calcium entry into renal vascular smooth muscle, thereby reducing the efficacy of vasoconstrictor hormones in regulation of renal blood flow and glomerular filtration rate. An alternative explanation is that nifedipine may inhibit the compensatory synthesis of vasodilatory prostaglandin E2 analogous to the clinical observation of acute deterioration in renal function by nonsteroidal anti-inflammatory drugs in patients with pre-existing renal insufficiency. These observations suggest that clinicians should monitor renal function closely and exercise caution when administering nifedipine to patients with underlying renal insufficiency.

Aged↗
PubMed1984

IgG-mediated intravascular hemolysis and nonoliguric acute renal failure complicating discontinuous rifampicin administration.

Acute renal failure following intermittent or discontinuous rifampicin therapy is a relatively infrequent clinical observation. Many pathogenetic mechanisms for the renal failure have been proposed, including intravascular hemolysis with hemoglobinuria and its consequent nephrotoxicity. We report the case of a patient who used rifampicin in a discontinuous fashion and developed hemolysis with nonoliguric acute renal failure. Most reported cases of antirifampicin antibodies are of the IgM class; thus, the development of an IgG antirifampicin antibody is of interest, especially because of its strong in vivo hemolytic properties. In addition, this patient developed a nonoliguric uremic course that did not require dialysis, both of which are distinctly unusual for this clinical setting.

Acute Kidney Injury↗
PubMed1982

Nonoliguric acute renal failure associated with a low fractional excretion of sodium.

Measurement of the fractional excretion of sodium has been recommended as a useful clinical tool in evaluating acute renal failure. Six patients with nonoliguric acute renal failure had a fractional excretion of sodium less than or equal to 1.0%; these patients had severe liver dysfunction, which suggested a sodium-avid state. A review of the literature showed that in patients with other sodium-avid states (congestive heart failure, nephrotic syndrome, and burns) the fractional excretion of sodium was frequently less than or equal to 1.0%. The fractional excretion of sodium is thus a less useful diagnostic test in patients whose clinical state makes them sodium avid.

Acute Kidney Injury↗
PubMed1982

Nonoliguric acute renal failure.

Nonoliguric acute renal failure is being recognized more commonly as a frequent initial observation for azotemia. Use of automated biochemical monitoring, aminoglycoside antibiotic utilization, and administration of potent diuretics and mannitol in settings of oliguria all contribute to its increased incidence. There appears to be less morbidity and mortality in patients with nonoliguric acute renal failure, and diagnostic urinary indexes suggest less of an insult to renal function. This article reviews the available literature and explores the reasons for the increased frequency of recognition of nonoliguric acute renal failure. Another aim is to compare nonoliguric acute renal failure with the oliguric from because there are important differences to be recognized by the clinician.

Acute Kidney Injury↗
PubMed1976

[Indications and contraindications for surgery in coronary insufficiency].

The indications to aortocoronary by-pass technique have during the last two years developed thanks to surgical, emodinamic and clinical exsperiences. The mortality of patients in whom surgery is limited electively to the intervention of aorto-coronary by-pass is at present around 4%. The principal indications to surgery are: a) existence of more than one coronary artery disease; b) a good diameter of the by-passing artery (more than 1 mm) corresponding to the site of the by-pass graft; c) a left ventricular telediastolic pressure lower than 20 mm of Hg; d) left ventricular function with ejection fraction not lesser than 0,40; e) absence of any associated severe and irreversible damages. The comparative data obtained recently from coronary patients medically and surgically treated would show at 4 years a survival rate higher than in those who underwent aorto-coronary by-pass.

Angina Pectoris↗
PubMed1976

[Surgical treatment of coronary insufficiency. Indications and contraindications (author's transl)].

The indications for surgical treatment by aortocoronary bypass have been considerably extended during the last few years as a result of experience in the clinical, hemodynamic and surgical fields. The mortality of the operation is about 4%. Important criteria are: 1. More than one coronary vessel must be affected. 2. The artery below the lesion must have a diameter of more than 1 mm. 3. The end-diastolic pressure in the left ventricle must be below 20 mm Hg. 4. The stroke volume fraction in the left ventricle must not be less than 0.40. 5. Serious intractable diseases must not be present.

Coronary Artery Bypass↗
PubMed1975

Centromeric and telomeric staining regions in the chromosomes of cattle (Bos taurus).

Two new types of staining regions exist aftet treatment with a modified version of the ammoniacal-silver technique (Howell et al., 1975), in addition to findings by many other researchers working on the chromosomal complement of Bos taurus. Densely stained regions appear to be associated with the centromeres of many of the 29 pairs of acrocentric chromosomes, but there are also 4-6 of the same acrocentric chromosomes bearing telomeric staining regions (TSRs) at the ends of their long arms. In many metaphases examined, actual physical connectives were observed between both types of these ammoniacal-silver staining regions.

Animals↗