Biomedical subjects

J Neugarten

Publications and source records attributed to J Neugarten.

46 records · Page 3Linked to original sources

PubMed1986

Amyloidosis in subcutaneous heroin abusers ("skin poppers' amyloidosis").

Systemic amyloidosis has recently emerged as a major cause of nephropathy among heroin abusers in New York City. Although focal glomerulosclerosis is typically seen in intravenous drug abusers who present with the nephrotic syndrome, those who escape this complication are at risk for the later development of amyloidosis related to their use of the subcutaneous route. Twenty such addicts identified between 1981 and 1984 are described. Patients typically present with chronic suppurative skin infections, edema, the nephrotic syndrome, benign urinary sediment, and normal-sized or enlarged kidneys. Tubular dysfunction, particularly renal tubular acidosis and diabetes insipidus, is frequent. Progression of renal insufficiency is characteristically rapid. Prolonged survival of heroin abusers and exhaustion of intravenous access requiring recourse to the subcutaneous route underlie the occurrence of amyloidosis in the addict population. Chronic suppurative skin infection consequent to repeated subcutaneous injection appears to be the underlying cause.

Adult↗

PubMed1985

Treatment of hypertension in renal disease.

Experimental and clinical evidence are summarized that support the hypothesis that enhanced transmission of systemic hypertension to the adapted glomerulus in the setting of reduced nephron mass may be responsible for accelerated vascular and glomerular damage in the hypertensive stage of parenchymal renal disease in man. In experimental models of hypertension associated with reduced renal mass, the kidney appears to be damaged directly by transmission of pressure rather than primarily through vasoconstriction and ischemia. When hypertension is combined with models of glomerular disease, vascular and glomerular injury are aggravated. It is proposed that adaptive glomerular hemodynamic alterations which occur in parenchymal renal disease magnify the transmission of increased pressure and flows when hypertension supervenes. Accelerated vascular and glomerular damage and functional deterioration result. According to this hypothesis, control of systemic hypertension and minimization of hydraulic stress on the diseased glomerulus become critical to the management of chronic renal disease and the prevention of progressive renal insufficiency.

Animals↗

PubMed1985

Nephrotoxic serum nephritis with hypertension: amelioration by antihypertensive therapy.

We have examined the effects of antihypertensive therapy on glomerular dynamics and on the clinical and morphologic features of a model of nephrotoxic serum nephritis (NSN) in which hypertension occurs. NSN was induced in uninephrectomized male Sprague Dawley rats, which drank 0.9% sodium chloride ad libitum. One-half were assigned randomly to a treated group whose blood pressure was normalized on a regimen of reserpine, hydralazine, and hydrochlorothiazide. Hypertension continued throughout the 6 weeks of study in untreated rats (blood pressure 148 +/- 5 vs. 103 +/- 3 mm Hg in treated rats, P less than 0.01). Urinary protein excretion was greater (437 +/- 110 vs. 254 +/- 81 mg/24 hr, P less than 0.005), and serum albumin lower (1.6 +/- 0.4 vs. 2.9 +/- 0.3 g/dl, P less than 0.01) in hypertensive animals. Diffuse glomerular endo- and extracapillary proliferation and arteriolar medial hypertrophy were observed frequently in nephritic rats with untreated hypertension. By contrast, structural abnormalities were limited primarily to focal segmental proliferation involving fewer than one-third of glomeruli in the absence of vascular changes in treated normotensive rats. Micropuncture studies performed 8 to 16 days after induction of nephritis showed a reduction in glomerular capillary pressure (46 +/- 1 vs. 55 +/- 1 mm Hg, P less than 0.001), glomerular plasma flow rate (115 +/- 20 vs. 160 +/- 20 nl/min, P less than 0.01), and single nephron filtration rate (42 +/- 4 vs. 56 +/- 5 nl/min, P less than 0.001) with antihypertensive treatment, suggesting that a hemodynamic mechanism may have been responsible for enhanced glomerular injury in the hypertensive nephritic animals.

Animals↗

PubMed1984

Glomerulonephritis in bacterial endocarditis.

The introduction of antibiotic therapy and changing epidemiologic patterns have altered the nature of glomerulonephritis as it occurs during the course of bacterial endocarditis. Observations made predominantly in the pre-antibiotic era suggested that infections with less virulent organisms, by virtue of their indolent subacute course, favored an antibody response predisposing to immune complex glomerulonephritis. Although antibiotic prophylaxis and therapy have reduced the incidence of both Streptococcus viridans bacterial endocarditis and concomitant glomerulonephritis, Staphylococcus aureus has become a major cause of acute bacterial endocarditis with a high incidence of glomerulonephritis. Parenteral drug abuse itself, which has emerged as a major factor predisposing to endocarditis, may also favor the development of glomerulonephritis. The course of glomerulonephritis has been altered in association with these changes in etiology and epidemiology. This review summarizes the clinical and morphologic features of glomerulonephritis as it currently occurs during the course of bacterial endocarditis.

Antigen-Antibody Complex↗

PubMed1984

Glomerulonephritis in bacterial endocarditis.

For a modern assessment of the clinical and morphologic features of glomerulonephritis accompanying bacterial endocarditis, postmortem and renal biopsy files were reviewed for the years 1965 to 1979, a period of changing epidemiology, etiology, and therapeutic regimens in infective endocarditis. The incidence of glomerulonephritis in 107 patients examined at postmortem was 22.4%; focal glomerulonephritis was present in 8.4%, diffuse glomerulonephritis in 14%. Glomerulonephritis occurred as frequently in acute as in subacute bacterial endocarditis. Staphylococcus aureus, which has replaced Streptococcus viridans as the predominant etiology of fatal bacterial endocarditis, was frequently associated with glomerulonephritis, especially in parenteral drug abusers. Renal functional impairment due to focal glomerulonephritis did not necessitate dialysis or contribute to the death of any patient. Presentation with advanced renal insufficiency due to diffuse glomerulonephritis was associated with both failure of antibiotic therapy to eradicate infection and failure to recover renal function. In patients with diffuse glomerulonephritis and less severe impairment of renal function, antibiotic therapy was successful in achieving bacteriologic cure, and complete recovery of renal function occurred in the majority. Features of persistent glomerular disease were frequent in patients with diffuse glomerulonephritis long after bacteriologic cure of endocarditis.

Adolescent↗

PubMed1983

Role of tubular obstruction in acute renal failure due to gentamicin.

Gentamicin sulfate was administered by intraperitoneal injection to male Sprague-Dawley rats in a dose of 100 to 120 mg/kg/day for 4 to 5 days to induce severe nephrotoxicity. In comparison to controls, inulin clearance was markedly decreased (2.87 +/- 0.31 vs. 8.65 +/- 0.31 ml/min/kg, P less than 0.001) as was urinary osmolality (462 +/- 36 vs. 1196 +/- 46, P less than 0.001). Surface tubules appeared heterogeneous. Some were plugged by whitish debris, whereas others were markedly dilated (I.D. = 41.5 +/- 2 mu). All other tubules were moderately dilated (I.D. = 28.8 vs. 20 mu). The microinfusion of tubules with cellular debris with an isotonic "equilibrium" solution resulted in a rise in intratubular pressure to as high as 60 to 80 mm Hg, compared with 13 to 15 mm Hg in normal rats. In better functioning nephrons, free-flow pressure (FFP) was increased significantly (16.0 +/- 0.5 vs. 10.2 +/- 0.1 mm Hg, P less than 0.001). Paired measurements of single nephron glomerular filtration rate (SNGFR) in these nephrons, made while monitoring intratubular pressure (ITP), revealed a rise in SNGFR when ITP was lowered from the initially high level to 10 mm Hg. Comparable changes in SNGFR were induced in normal rats by varying ITP from 10 to 15 mm Hg. The data suggest that in severe gentamicin nephrotoxicity, many cortical nephrons may be contributing very little to excretory function, presumably because of intratubular obstruction. The less impaired nephrons have reduced SNGFR, due in part to increased free-flow pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗

PubMed1983

Amelioration of experimental glomerulonephritis by dietary protein restriction.

We have examined the effects of various levels of dietary protein intake on the course of nephrotoxic serum nephritis in the rat by feeding low (4.6% casein), standard (23% casein), and high (57.5% casein) protein diets which were identical in calorie, mineral, and electrolyte content. Nephritic rats on a high protein diet manifested heavy proteinuria, hypoalbuminemia, hypercholesterolemia, azotemia, and elevated serum creatinine levels. In those subjected to dietary protein restriction, proteinuria remitted and azotemia did not develop. While mesangial widening, interstitial abnormalities, and segmental proliferation and sclerosis of glomeruli occurred regularly in nephritic rats fed high protein diets, histologic abnormalities were virtually absent in those on low protein intake. Animals on a standard protein intake manifested histologic and clinical features intermediate in severity. We conclude that the renal functional and histologic consequences of nephrotoxic serum nephritis can be averted by dietary protein restriction.

Animals↗

PubMed1982

Aggravation of experimental glomerulonephritis by superimposed clip hypertension.

To evaluate the possible enhancing effect of hypertension on the clinical and morphologic features of glomerulonephritis, two-kidney clip hypertension (CH) was superimposed on a mild form of nephrotoxic serum nephritis (NSN) in female Sprague-Dawley rats. The following parameters were assessed regularly over a 6-month period: blood pressure (BP), heart weight, proteinuria (UpV), and renal morphology. Blood pressure and heart weights were increased equally in clip hypertension and in nephrotoxic serum nephritis combined with clip hypertension. While only moderate proteinuria occurred in nephrotoxic serum nephritis (49 +/- 28 mg/24 hr) or clip hypertension (40 +/- 22 mg/24 hr) alone, the superimposition of clip hypertension on nephrotoxic serum nephritis resulted in heavy proteinuria (161 +/- 36 mg/24 hr) (P less than 0.001) after 5 months of hypertension. Glomerular histology in nephrotoxic serum nephritis showed infrequent focal and segmental proliferation and minimal sclerosis; vessels were normal. Clip hypertension was characterized by infrequent and mild vascular sclerosis and glomerular proliferation and sclerosis. Severe glomerular endo- and extracapillary proliferation and widespread glomerular and vascular sclerosis occurred in the majority of rats when nephrotoxic serum nephritis was combined with clip hypertension. The data demonstrate that clip hypertension enhances glomerular proliferation and sclerosis and results in the development of vascular sclerosis in experimental nephritis.

Animals↗

PubMed1978

Chronic active hepatitis and ulcerative colitis associated with eosinophilia, nonthrombocytopenic hypergammaglobulinemic purpura and serologic abnormalities.

A patient with chronic active hepatitis (CAH) and ulcerative colitis (UC) associated with eosinophilia, nonthrombocytopenic hypergammaglobulinemic purpura and serologic abnormalities is presented. Abnormal liver function, gastrointestinal and systemic symptoms as well as the associated epiphenomena responded dramatically to oral corticosteroid therapy. The remission was maintained during an eight month follow-up period with low dose prednisone therapy.

Adult↗

PubMedDate not supplied

Rifampin-induced nephrotic syndrome and acute interstitial nephritis.

The occurrence of renal insufficiency associated with heavy glomerular proteinuria during the course of continuous rifampin therapy in a patient with pulmonary tuberculosis is reported. Renal biopsy demonstrated acute interstitial nephritis, normal glomerular histology, effacement of glomerular epithelial cell foot processes, and electron-dense deposits in mesangial matrix and subendothelial and paramesangial sites. Discontinuation of rifampin was followed by improvement in renal function and abatement of proteinuria. We call attention to the broad clinical and morphologic spectrum of nephrotoxicity which may be induced by rifampin and a variety of other drugs.

Acute Disease↗