Biosketch / Results /
Robert G Schacht, M.D.
Clinical Professor; Division Director of Pediatric NephrologyDepartment of Pediatrics (Pediatrics)
NYU Pediatric Cardiology
Clinical Addresses
530 FIRST AVENUE, SUITE 9USKIRBALL INSTITUTE
NEW YORK, NY 10016
Phone: 212-263-5940
Fax: 212-263-5808
Medical Specialties
General Pediatrics, Pediatric NephrologyMedical Expertise
Pediatric NephrologyInsurance
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Board Certification
1971 — Pediatrics1974 — Pediatric Nephrology (Peds)
Education
1966 — Creighton University School of Medicine, Medical Education1966-1969 — NYU Medical Center (Pediatrics), Residency Training
1969-1971 — NYU Medical Center (Nephrology), Clinical Fellowships
All data from NYU Health Sciences Library Faculty Bibliography — -
Contact:
http://hsl.med.nyu.edu/faculty-bibliography-search#about
Cutaneous anthrax associated with microangiopathic hemolytic anemia and coagulopathy in a 7-month-old infant
Freedman, Abigail; Afonja, Olubunmi; Chang, Mary Wu; Mostashari, Farzad; Blaser, Martin; Perez-Perez, Guillermo; Lazarus, Herb; Schacht, Robert; Guttenberg, Jane; Traister, Michael; Borkowsky, William
2002 Feb 20;287(7):869-874, JAMA
A 7-month-old infant with cutaneous anthrax developed severe systemic illness despite early treatment with antibiotics. The infant displayed severe microangiopathic hemolytic anemia with renal involvement, coagulopathy, and hyponatremia. These findings are unusual with cutaneous anthrax, but have been described in illness resulting from spider toxin and may delay correct diagnosis. The systemic manifestations of the disease persisted for nearly a month despite corticosteroid therapy, but resolved
—
id: 26017,
year: 2002,
vol: 287,
page: 869,
stat: Journal Article,
Very low birth weight infants - a new hypertensive population?
Kim, YS; Wang, J; Hendricks-Munoz, KD; Schacht, RG
1999 APR ;45(4):247A-247A, Pediatric research
—
id: 54069,
year: 1999,
vol: 45,
page: 247A,
stat: Journal Article,
Primary peritonitis as a presenting feature of nephrotic syndrome: a case report and review of the literature
Markenson DS; Levine D; Schacht R
1999 Dec;15(6):407-409, Pediatric emergency care
—
id: 11896,
year: 1999,
vol: 15,
page: 407,
stat: Journal Article,
Renal blood flow velocity in neonates with and without umbilical artery catheters
Glickstein JS; Rutkowski M; Schacht R; Friedman D
1994 Nov-Dec;22(9):543-550, Journal of clinical ultrasound
We performed an observational prospective cohort study on the applicability of two-dimensional echocardiography with pulsed Doppler technique as a noninvasive modality to serially evaluate renal blood velocities in premature neonates with and without umbilical artery catheters. We also sought to determine the incidence of umbilical artery catheter-related thrombus formation in our neonatal intensive-care unit. We established normative values for renal artery blood flow velocities in premature neonates and postulate that this echo-Doppler technique is valid and can be used to evaluate renal developmental physiology in the neonatal population. In addition, we observed that even in the absence of clinical sequelae due to thrombus formation, the presence of a thrombus in the aorta caused abnormalities in renal hemodynamics
—
id: 6627,
year: 1994,
vol: 22,
page: 543,
stat: Journal Article,
Doppler waveforms in the renal arteries of normal children
Friedman DM; Schacht RG
1991 Sep;19(7):387-392, Journal of clinical ultrasound
Blood velocity waveforms in peripheral arteries vary such that decreasing vascular resistance results in a relative increase in diastolic velocity at steady state. We measured blood velocity in renal arteries of 20 children (age: 119 months +/- 37 months; weight: 38 kg +/- 15 kg) to establish normal values, and to explore the relationship between these waveforms and central hemodynamics. Using image-directed pulsed Doppler echocardiography, M-mode measurements and cardiac index were recorded. Renal hila were visualized via the flank for Doppler sampling. Peak systolic velocity (A) and minimal diastolic velocity (B) were determined. The results (mean +/- SD) were as follows: Renal artery A/B = 2.9 +/- 0.74 (range 1.9 to 5.1). Characteristic waveforms were identical bilaterally and had continuous diastolic forward flow: A/B was independent of central hemodynamics within the resting normal range, varying inversely with age and size
—
id: 13932,
year: 1991,
vol: 19,
page: 387,
stat: Journal Article,
RENAL-ARTERY DOPPLER WAVE-FORMS IN NEONATES WITH UMBILICAL ARTERY CATHETERS
GLICKSTEIN, J; FRIEDMAN, D; SCHACHT, R; RUTKOWSKI, M
1991 OCT ;39(3):A669-A669, Clinical research
—
id: 51550,
year: 1991,
vol: 39,
page: A669,
stat: Journal Article,
Dietary protein restriction and glomerular permselectivity in nephrotoxic serum nephritis
Neugarten J; Kozin A; Gayner R; Schacht RG; Baldwin DS
1991 Jul;40(1):57-61, Kidney international
We have previously demonstrated that long-term dietary protein restriction ameliorates proteinuria and limits glomerular structural injury in rats with nephrotoxic serum nephritis. In the present study, we examined the influence of short-term dietary protein restriction on glomerular permselectivity. As compared to nephritic rats maintained on a normal protein diet, whole kidney and single nephron hemodynamics were lower in nephritic rats subjected to dietary protein restriction of three days duration (glomerular filtration rate: 0.79 +/- 0.10 vs. 1.46 +/- 0.11 ml/min, P less than 0.003; renal plasma flow rate: 2.50 +/- 0.34 vs. 3.96 +/- 0.38 ml/min, P less than 0.02; glomerular capillary pressure: 44 +/- 1 vs. 53 +/- 1 mm Hg, P less than 0.002; proteinuria: 77 +/- 15 vs. 224 +/- 14 mg/24 hr, P less than 0.01). This was associated with a rise in afferent resistance, from 2.99 +/- 0.77 to 5.45 +/- 0.94 dyn.sec.cm-5, NS. In nephritic rats maintained on 24% protein, fractional clearances were elevated above control values for neutral dextrans with molecular radii exceeding 50 A but were depressed for those with molecular radii below 30 A (P less than 0.05). Dietary protein restriction elevated the fractional clearances of dextrans with radii less than 30 A while depressing the fractional clearances of dextrans with radii greater than 50 A (P less than 0.05). The proportion of glomerular filtrate permeating the shunt pathway was elevated above control values in nephritic rats on the 24% protein diet but declined in those fed the low protein diet (NSN-24%: 0.86%; NSN-6%: 0.31%; control: 0.19%).(ABSTRACT TRUNCATED AT 250 WORDS)
—
id: 65158,
year: 1991,
vol: 40,
page: 57,
stat: Journal Article,
DOPPLER WAVE-FORMS IN THE RENAL-ARTERY OF NORMAL-CHILDREN
Friedman, DM; Schacht, RG
1990 Apr;27(4):A328-A328, Pediatric research
—
id: 31993,
year: 1990,
vol: 27,
page: A328,
stat: Journal Article,
SYSTEMIC HYPERTENSION IN AN INFANT WITH RENAL-ARTERY EMBOLISM FOLLOWING UMBILICAL ARTERY CATHETERIZATION - A CASE-REPORT DESCRIBING EVALUATION BY RENAL-ARTERY DOPPLER TECHNIQUE
Friedman, DM; Schacht, RG; Rutkowski, M
1990 Fall;9(2):137-141, Journal of cardiovascular technology
—
id: 31824,
year: 1990,
vol: 9,
page: 137,
stat: Journal Article,
Rapid renal failure in AIDS-associated focal glomerulosclerosis
Langs C; Gallo GR; Schacht RG; Sidhu G; Baldwin DS
1990 Feb;150(2):287-292, Archives of internal medicine
We studied the clinical features, pathologic findings, and course of 18 patients who were found to have glomerular disease at the time of hospitalization with manifestations of acquired immunodeficiency syndrome or acquired immunodeficiency syndrome-related complex at New York University Medical Center, New York, NY, during 1984 through 1987. Focal glomerulosclerosis, characterized by segmental and/or global collapse of capillary walls, was observed in 15 of these patients; mesangial proliferation in 2, and membranous nephropathy in 1. Those with focal glomerulosclerosis typically demonstrated heavy proteinuria without edema or hypertension and progressed rapidly to renal failure in less than 1 year from the time of discovery. This form of focal glomerulosclerosis is characterized by a fulminant course, the collapse type of sclerosis, and the frequent occurrence of uremia without advanced glomerular obliteration. The absence of widespread glomerular sclerosis and the rapid course suggest that unique renal hemodynamic mechanisms may be responsible for the progression
—
id: 59940,
year: 1990,
vol: 150,
page: 287,
stat: Journal Article,
Glomerular size-selective barrier dysfunction in nephrotoxic serum nephritis
Alfino PA; Neugarten J; Schacht RG; Dworkin LD; Baldwin DS
1988 Aug;34(2):151-155, Kidney international
We have previously reported amelioration of heavy proteinuria, vascular sclerosis and glomerular structural damage by antihypertensive therapy in nephrotoxic serum nephritis (NSN). In the present study, we examine glomerular permselectivity in this hypertensive form of NSN and the effect of hypertension treatment on size-selective barrier function. Mean arterial pressure was maintained at normotensive levels (mean 123 +/- 3 mm Hg) with a combination of hydralazine, hydrochlorthiazide and reserpine in 7 nephritic rats, while 10 untreated rats remained hypertensive (mean 165 +/- 4 mm Hg). At six weeks, glomerular filtration rate was reduced in untreated rats (mean 0.54 ml/min) but was preserved in those rendered normotensive (mean 1.71 ml/min), P less than 0.02). Twenty-four-hour urinary protein excretion, mean 371 +/- 74 mg in hypertensive nephritic rats, was markedly reduced in rats on the antihypertensive regimen to a mean of 120 +/- 17 mg (P less than 0.02), as was 24-hour urinary gamma-globulin excretion (mean 35 +/- 9 mg in untreated vs. 16 +/- 2 mg in treated). Fractional clearances of tritiated polydisperse neutral dextrans were significantly enhanced for molecular radii exceeding 50 angstroms in hypertensive animals, indicative of a loss of glomerular size permselectivity. Rats on antihypertensive therapy did not develop such a size selective defect. Thus, hypertensive rats with nephrotoxic serum nephritis develop 'gaps' in the glomerular basement membrane which allow the excretion of large molecular weight neutral dextrans and gamma-globulin. This defect in glomerular permselectivity can be averted with antihypertensive therapy
—
id: 11027,
year: 1988,
vol: 34,
page: 151,
stat: Journal Article,
RAPID RENAL-FAILURE IN AIDS NEPHROPATHY
LANGS, C; GALLO, GR; SCHACHT, RG; BALDWIN, DS
1988 JAN ;33(1):198-198, Kidney international
—
id: 41833,
year: 1988,
vol: 33,
page: 198,
stat: Journal Article,
Nephrotoxic serum nephritis with hypertension: perfusion pressure and permselectivity
Neugarten J; Alfino P; Langs C; Schacht RG; Baldwin DS
1988 Jan;33(1):53-57, Kidney international
We examined the effect of acute reduction in renal perfusion pressure on proteinuria and glomerular permselectivity in a model of nephrotoxic serum nephritis which is characterized by hypertension, heavy proteinuria and severe structural injury. Sequential dextran sieving studies were performed after two weeks of nephritis in 10 uninephrectomized rats at their basal elevated blood pressure levels (154 +/- 3 mm Hg) and at lowered renal perfusion pressure of 105 to 110 mm Hg, achieved by adjusting a ligature around the aorta above the origin of the renal artery. Glomerular filtration rate (GFR) decreased from 1.35 +/- 0.24 to 0.95 +/- 0.19 ml/min (P less than 0.002), while urinary protein excretion (factored for filtration rate) declined from 0.69 +/- 0.2 to 0.39 +/- 0.1 mg per ml GFR (P less than 0.002) at the lower perfusion pressure. A companion protocol documented a modest reduction in renal plasma flow (RPF) from 4.96 +/- 0.48 to 4.44 +/- 0.63 ml/min (P less than 0.05) and a decline in glomerular transcapillary hydraulic pressure difference (delta P) from 43 to 33 mm Hg (P less than 0.001) during the ligature maneuver. In the hypertensive state, fractional clearances of neutral dextrans (theta ND) with molecular radii exceeding 40 A were elevated in nephritic rats as compared to uninephrectomized non-nephritic controls. With reduction in renal perfusion pressure. Theta ND uniformly declined toward control values and remained significantly elevated only for molecular radii exceeding 55 A. The calculated fraction of glomerular filtrate passing through a non-size discriminatory shunt, pathway was 0.93% during the hypertensive period and was reduced at lower perfusion pressures to 0.52% (to be compared to 0.19% in controls).(ABSTRACT TRUNCATED AT 250 WORDS)
—
id: 11292,
year: 1988,
vol: 33,
page: 53,
stat: Journal Article,
PRESERVATION OF GLOMERULAR SIZE-SELECTIVE BARRIER BY ANTIHYPERTENSIVE THERAPY IN NEPHROTOXIC SERUM NEPHRITIS (NSN)
Alfino, P; Neugarten, J; Schacht, RG; Dworkin, L; Baldwin, DS
1987 Jan;31(1):379-379, Kidney international
—
id: 31420,
year: 1987,
vol: 31,
page: 379,
stat: Journal Article,
ACUTE REDUCTION IN BLOOD-PRESSURE REVERSES SIZE-SELECTIVE BARRIER DYSFUNCTION IN HYPERTENSIVE NEPHROTOXIC SERUM NEPHRITIS (NSN)
Neugarten, J; Alfino, P; Schacht, RG; Baldwin, DS
1987 Jan;31(1):305-305, Kidney international
—
id: 31294,
year: 1987,
vol: 31,
page: 305,
stat: Journal Article,
RESTORATION OF GLOMERULAR SIZE SELECTIVE BARRIER BY ANTIHYPERTENSIVE THERAPY IN NEPHROTOXIC SERUM NEPHRITIS (NSN)
Alfino, P; Neugarten, J; Schacht, RG; Dworkin, L; Baldwin, DS
1986 Dec;4(4):S565-S565, Journal of hypertension
—
id: 31401,
year: 1986,
vol: 4,
page: S565,
stat: Journal Article,
FAILURE TO AUTOREGULATE FILTRATION-RATE IN EXPERIMENTAL GLOMERULONEPHRITIS
Langs, C; Neugarten, J; Schacht, RG; Baldwin, DS
1986 Jan;29(1):322-322, Kidney international
—
id: 31095,
year: 1986,
vol: 29,
page: 322,
stat: Journal Article,
ROLE OF HYPERPHAGIA IN EXPERIMENTAL DIABETIC NEPHROPATHY
Neugarten, J; Liu, D; Feiner, H; Schacht, RG; Baldwin, DS
1986 Jan;29(1):324-324, Kidney international
—
id: 31096,
year: 1986,
vol: 29,
page: 324,
stat: Journal Article,
ROLE OF HYPERPHAGIA IN EXPERIMENTAL DIABETIC NEPHROPATHY
NEUGARTEN, J; LIU, D; FEINER, H; SCHACHT, RG; BALDWIN, DS
1986 APR ;34(2):A604-A604, Clinical research
—
id: 41403,
year: 1986,
vol: 34,
page: A604,
stat: Journal Article,
Nephrotoxic serum nephritis with hypertension: amelioration by antihypertensive therapy
Neugarten J; Kaminetsky B; Feiner H; Schacht RG; Liu DT; Baldwin DS
1985 Aug;28(2):135-139, Kidney international
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
—
id: 65163,
year: 1985,
vol: 28,
page: 135,
stat: Journal Article,
NEPHROTOXIC SERUM NEPHRITIS (NSN) WITH HYPERTENSION - AMELIORATION BY ANTIHYPERTENSIVE THERAPY
Neugarten, J; Kaminetsky, B; Feiner, H; Schacht, RG; Baldwin, DS
1985 ;27(1):248-248, Kidney international
—
id: 30989,
year: 1985,
vol: 27,
page: 248,
stat: Journal Article,
Amelioration of experimental glomerulonephritis by dietary protein restriction
Neugarten J; Feiner HD; Schacht RG; Baldwin DS
1983 Nov;24(5):595-601, Kidney international
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
—
id: 65180,
year: 1983,
vol: 24,
page: 595,
stat: Journal Article,
AGGRAVATION OF EXPERIMENTAL DIABETIC NEPHROPATHY BY HIGH DIETARY-PROTEIN
NEUGARTEN, J; LIU, D; FEINER, H; SCHACHT, R; CHUBA, J; BALDWIN, DS
1983 ;31(2):A438-A438, Clinical research
—
id: 40547,
year: 1983,
vol: 31,
page: A438,
stat: Journal Article,
The effect of lithium on renal haemodynamic function
Tyrer, S P; Schacht, R G; McCarthy, M J; Menard, K N; Leong, S; Shopsin, B
1983 Feb;13(1):61-69, Psychological medicine
Renal concentrating capacity following 18 hours of fluid deprivation was measured in 75 patients receiving prophylactic lithium therapy, and in 30 affectively ill subjects receiving other drugs. The lithium-treated patients had significantly lower urine osmolality and higher serum osmolality than the control subjects. Older subjects, patients maintained at higher serum lithium levels and those with a history of previous neurotoxicity showed the most impairment. Ten patients with urine osmolalities of less than 700 mOsm/1 following this test were investigated further. Inulin and para-amino hippurate (PAH) clearance rates were determined and the effect of a subpressor challenge of dopamine on these measures was observed. Half of the patients showed some reduction in inulin and PAH clearance, which was greatest in those patients who had been taking lithium for over 10 years. However, all of the patients tested showed the expected increase in renal blood flow and sodium and water excretion in response to dopamine. Six additional patients had clearance estimations made before starting lithium treatment which were repeated after a period of 3-6 months on the drug. No consistent changes in haemodynamics were observed. Lithium clearly reduces renal concentrating capacity, but other measures of renal tubular function were well preserved in patients receiving long-term therapy. Glomerular function may be slightly reduced in patients taking lithium for long periods. The results show that prophylactic lithium treatment does not affect renal cortical function adversely in the majority of patients, but impaired renal concentrating ability is a common accompaniment
—
id: 105003,
year: 1983,
vol: 13,
page: 61,
stat: Journal Article,
Intrarenal vascular sclerosis in IgA nephropathy
Feiner HD; Cabili S; Baldwin DS; Schacht RG; Gallo GR
1982 Oct;18(4):183-192, Clinical nephrology
In this analysis of 43 patients with IgA nephropathy, renal morphology was correlated with clinical data. Gross hematuria and mild proteinuria were typical among younger patients. Among older individuals the clinical spectrum was wider. A comparison with data previously obtained from the normal population indicated that disease-related glomerular sclerosis was present in 1/3 of initial biopsy specimens. The prevalent pattern of glomerular sclerosis was that of global tuft collapse, the type of sclerosis known to result from ischemia. Intrarenal vascular sclerosis was present in 1/3 of initial biopsies. Follow-up specimens from 6 patients showed progression of glomerular sclerosis, vascular sclerosis or both. Hypertension occurred in over 1/4 of patients. It is proposed that progressive renal damage in IgA nephropathy may not be solely immunologically mediated. Glomerular sclerosis may also be mediated by vascular sclerosis, or alterations in intrarenal hemodynamics in glomerulonephritis may have a direct damaging effect on both the glomerulus and the intrarenal vasculature
—
id: 59966,
year: 1982,
vol: 18,
page: 183,
stat: Journal Article,
Aggravation of experimental glomerulonephritis by superimposed clip hypertension
Neugarten J; Feiner HD; Schacht RG; Gallo GR; Baldwin DS
1982 Sep;22(3):257-263, Kidney international
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
—
id: 59967,
year: 1982,
vol: 22,
page: 257,
stat: Journal Article,
AMELIORATIVE EFFECT OF DIETARY-PROTEIN RESTRICTION ON THE COURSE OF NEPHROTOXIC SERUM NEPHRITIS
NEUGARTEN, J; FEINER, H; SCHACHT, RG; BALDWIN, DS
1982 JAN 20 ;30(2):A541-A541, Clinical research
—
id: 98623,
year: 1982,
vol: 30,
page: A541,
stat: Journal Article,
Renal failure in minimal change nephrotic syndrome
Lowenstein J; Schacht RG; Baldwin DS
1981 Feb;70(2):227-233, American journal of medicine
Renal insufficiency, with serum creatinines ranging from 2.3 to 13.4 mg/dl, was observed in 15 patients with the minimal change nephrotic syndrome. Recovery of renal function occurred in association with diuretic therapy in 13, eight of whom subsequently underwent steroid-induced remission of the nephrotic syndrome. Two patients failed to undergo diuresis or to have a remission of the nephrotic syndrome and died with persistent renal failure. Glomerular filtration rate (Cinulin) was reduced out of proportion to renal plasma flow (CPAH) as evidenced by remarkably low filtration fractions ranging from 0.03 to 0.095. The invariable association between diuresis and recovery of renal function, the recurrence of renal failure when fluid reaccumulated and the finding of markedly depressed filtration fractions lead us to postulate that renal failure in minimal change nephrotic syndrome may be due to a reversible alteration in glomerular hemodynamics which is related to fluid retention and associated intrarenal edema
—
id: 65186,
year: 1981,
vol: 70,
page: 227,
stat: Journal Article,
AGGRAVATION OF EXPERIMENTAL GLOMERULONEPHRITIS BY SUPERIMPOSED CLIP HYPERTENSION
Neugarten, J; Feiner, H; Schacht, RG; Gallo, GR; Baldwin, DS
1981 ;19(1):188-188, Kidney international
—
id: 30289,
year: 1981,
vol: 19,
page: 188,
stat: Journal Article,
Nephrotoxicity of nitrosoureas
Schacht RG; Feiner HD; Gallo GR; Lieberman A; Baldwin DS
1981 Sep 15;48(6):1328-1334, Cancer
Irreversible and progressive renal parenchymal damage and functional impairment occurred in the majority of patients receiving at least six courses (200 mg/m2 of BCNU and/or methyl CCNU at eight-week intervals) of nitrosoureas for therapy of malignant brain tumors. Seventeen of 18 patients who received at least six courses and all nine patients who received more than ten courses developed impaired renal function as judged by elevation of blood urea nitrogen and/or serum creatinine or decrease in filtration rate as determined by inulin clearance. Four patients have developed uremia. Renal tissue obtained from seven patients demonstrated tubular atrophy, interstitial fibrosis and glomerular sclerosis. This remarkably high incidence of renal damage occurred without a phase of acute renal failure and in the absence of significant urinary abnormalities, while producing an insidiously progressive interstitial renal lesion
—
id: 59970,
year: 1981,
vol: 48,
page: 1328,
stat: Journal Article,
RENAL FUNCTIONAL IMPAIRMENT IN DYSAUTONOMIA
Schacht, RG; Baldwin, DS
1981 ;19(1):137-137, Kidney international
—
id: 30286,
year: 1981,
vol: 19,
page: 137,
stat: Journal Article,
ENHANCED LYMPHOBLASTIC TRANSFORMATION IN RESPONSE TO GLYCOSIDASE TREATED GLOMERULAR BASEMENT-MEMBRANE (GBM) IN MINIMAL CHANGE NEPHROTIC SYNDROME (MCNS)
Cabili, S; Spinowitz, B; Schacht, RG; Obiedzinski, G; Gombos, EA; Baldwin, DS
1980 ;28(2):A440-A440, Clinical research
—
id: 28010,
year: 1980,
vol: 28,
page: A440,
stat: Journal Article,
INTRA-RENAL VASCULAR-DISEASE IN BERGER IGA NEPHROPATHY (BN)
Feiner, HD; Cabili, S; Baldwin, DS; Schacht, RG; Gallo, GR
1980 ;42(Suppl 1):116-116, Laboratory investigation
—
id: 28042,
year: 1980,
vol: 42,
page: 116,
stat: Journal Article,
Role of intrarenal vascular sclerosis in progression of poststreptococcal glomerulonephritis
Gallo GR; Feiner HD; Steele JM Jr; Schacht RG; Gluck MC; Baldwin DS
1980 Feb;13(2):49-57, Clinical nephrology
A comparison has been made of the percentage of sclerotic glomeruli found in normal subjects and in 31 patients 6 months to 15 years after an episode of acute poststreptococcal glomerulonephritis (PSGN). The findings establish that a greater than expected incidence of glomerular sclerosis occurs in the course of PSGN. The pattern of glomerular sclerosis frequently was that of contracted collapsed tufts, one known to result from ischemia. In the majority of specimens with significant glomerular sclerosis, there was co-existent vascular sclerosis (arterioles and/or prearterioles), and the incidence of both glomerular and vascular sclerosis increased with time from onset of PSGN. Intrarenal vascular sclerosis may thus be of major importance in the genesis and progression of glomerular sclerosis in PSGN
—
id: 59974,
year: 1980,
vol: 13,
page: 49,
stat: Journal Article,
SEVERE RENAL-DISEASE - A NEW MANIFESTATION OF FAMILIAL DYSAUTONOMIA
Schacht, RG; Axelrod, F
1980 ;14(4):625-625, Pediatric research
—
id: 28136,
year: 1980,
vol: 14,
page: 625,
stat: Journal Article,
Lithium and the kidney
Tyrer, S P; McCarthy, M J; Shopsin, B; Schacht, R G
1980 Jan 12;1(8159):94-95, Lancet
—
id: 104996,
year: 1980,
vol: 1,
page: 94,
stat: Journal Article,
ENHANCED LYMPHOBLASTIC TRANSFORMATION IN RESPONSE TO GLYCOSIDASE TREATED GLOMERULAR BASEMENT-MEMBRANE (GBM) IN MINIMAL CHANGE NEPHROTIC SYNDROME (MCNS)
Cabili, S; Spinowitz, B; Schacht, RG; Obiedzinski, G; Gombos, EA; Baldwin, DS
1979 ;16(6):927-927, Kidney international
—
id: 30063,
year: 1979,
vol: 16,
page: 927,
stat: Journal Article,
INTRA-RENAL VASCULAR-DISEASE IN BERGERS NEPHROPATHY
Feiner, HD; Cabili, S; Gallo, GR; Schacht, RG; Baldwin, DS
1979 ;16(6):929-929, Kidney international
—
id: 30064,
year: 1979,
vol: 16,
page: 929,
stat: Journal Article,
Lymphocyte subpopulations in minimal change nephrotic syndrome
Kerpen HO; Bhat JG; Kantor R; Gauthier B; Rai KR; Schacht RG; Baldwin DS
1979 Sep;14(1):130-136, Clinical immunology & immunopathology
—
id: 65159,
year: 1979,
vol: 14,
page: 130,
stat: Journal Article,
Irreversible disease following acute poststreptococcal glomerulonephritis in children
Schacht RG; Gallo GR; Gluck MC; Iqbal MS; Baldwin DS
1979 ;32(7):515-524, Journal of chronic diseases
—
id: 59976,
year: 1979,
vol: 32,
page: 515,
stat: Journal Article,
LYMPHOCYTE SUB-POPULATIONS IN MINIMAL CHANGE NEPHROTIC SYNDROME (MCNS)
Spinowitz, BS; Cabili, S; Schacht, RG; Obiedzinski, G; Gombos, EA; Baldwin, DS
1979 ;16(6):913-913, Kidney international
—
id: 30062,
year: 1979,
vol: 16,
page: 913,
stat: Journal Article,
INTERSTITIAL NEPHRITIS, A REVERSIBLE CAUSE OF RENAL-FAILURE IN SARCOIDOSIS
Abularrage, JJ; Szer, IS; Matthews, MJ; Schacht, RG
1978 ;12(4):537-537, Pediatric research
—
id: 29941,
year: 1978,
vol: 12,
page: 537,
stat: Journal Article,
DOUBLE-MARKED LYMPHOCYTES IN MINIMAL CHANGE NEPHROTIC SYNDROME (MCNS)
Bhat, JG; Kerpen, HO; Schacht, RG; Gombos, EA; Spinowitz, B; Handelsman, S; Rai, C; Gauthier, B; Kantor, C; Baldwin, DS
1978 ;12(4):539-539, Pediatric research
—
id: 29942,
year: 1978,
vol: 12,
page: 539,
stat: Journal Article,
DOUBLE-MARKED LYMPHOCYTES IN MINIMAL CHANGE NEPHROTIC SYNDROME (MCNS)
Bhat, JG; Kerpen, HO; Schacht, RG; Rai, K; Gauthier, B; Kanter, RJ; Baldwin, DS
1978 ;26(3):A457-A457, Clinical research
—
id: 29924,
year: 1978,
vol: 26,
page: A457,
stat: Journal Article,
ROLE OF INTRA-RENAL VASCULAR SCLEROSIS IN PROGRESSION OF POSTSTREPTOCOCAL GLOMERULONEPHRITIS (PSGN)
Gallo, GR; Feiner, HD; Schacht, RG; Gluck, MC; Baldwin, DS
1978 ;26(3):A462-A462, Clinical research
—
id: 29814,
year: 1978,
vol: 26,
page: A462,
stat: Journal Article,
Plasma renin and serum dopamine-beta-hydroxylase during orthostatic hypotension in quadriplegic man
Kamelhar DL; Steele JM Jr; Schacht RG; Lowenstein J; Naftchi NE
1978 May;59(5):212-216, Archives of physical medicine & rehabilitation
To determine whether orthostatic hypotension in patients with cervical spinal cord lesions is the result of impaired sympathetic nerve response and/or impaired renin release, serum dopamine-beta-hydroxylase (DbetaH) activity and plasma renin activity (PRA) were examined during passive tilting in 6 quadriplegic patients and in 6 able-bodied control subjects. Serum DbetaH was measured by an isotopic enzymatic method and PRA by radioimmunoassay. Following head-up tilting, quadriplegic subjects demonstrated a prompt, significant decrease in mean arterial pressure (MAP) and increase in heart rate (HR). DbetaH and PRA both increased significantly 15 minutes after tilt. In normal subjects, although HR increased, MAP was unchanged; DbetaH and PRA did not increase significantly during head-up tilt. The finding of increased DbetaH during tilt hypotension in quadriplegic patients provides evidence that reflex sympathetic nerve stimulation persists despite cervical cord transection. Increased PRA may be attributed to decreased renal perfusion pressure and increased sympathetic stimulation during tilt hypotension. These data suggest that orthostatic hypotension in quadriplegia patients cannot be attributed solely to failure of the sympathetic nervous system or the renin-angiotensin system to respond to the stimulus of orthostasis
—
id: 20318,
year: 1978,
vol: 59,
page: 212,
stat: Journal Article,
RENAL-FAILURE IN MINIMAL CHANGE NEPHROTIC SYNDROME (MCNS)
Lowenstein, J; Schacht, RG; Baldwin, DS
1978 ;14(6):656-656, Kidney international
—
id: 30163,
year: 1978,
vol: 14,
page: 656,
stat: Journal Article,
CHRONIC INTERSTITIAL NEPHRITIS AND RENAL-FAILURE DUE TO NITROSOUREA (NU) THERAPY
Schacht, RG; Baldwin, DS
1978 ;14(6):661-661, Kidney international
—
id: 30054,
year: 1978,
vol: 14,
page: 661,
stat: Journal Article,
FAILURE OF KIDNEY TO VASODILATE IN DIABETES-MELLITUS
Schacht, RG; Baldwin, DS
1978 ;26(3):A475-A475, Clinical research
—
id: 29925,
year: 1978,
vol: 26,
page: A475,
stat: Journal Article,
FAILURE OF KIDNEY TO VASODILATE IN DIABETES-MELLITUS
Schacht, RG; Baldwin, DS
1978 ;12(4):547-547, Pediatric research
—
id: 29943,
year: 1978,
vol: 12,
page: 547,
stat: Journal Article,
LONG-TERM COURSE OF POST-STREPTOCOCCAL GLOMERULONEPHRITIS (PSGN)
Schacht, RG; Gallo, GR; Gluck, MC; Feiner, HD; Baldwin, DS
1978 ;26(3):A544-A544, Clinical research
—
id: 29930,
year: 1978,
vol: 26,
page: A544,
stat: Journal Article,
ROLE OF INTRA-RENAL VASCULAR SCLEROSIS IN PROGRESSION OF POST-STREPTOCOCCAL GLOMERULONEPHRITIS (PSGN)[Abstract]
Gallo, GR; Feiner, HD; Schacht, RG; Gluck, MC; Baldwin, DS
1977 ;12(6):512-512, Kidney international
—
id: 29859,
year: 1977,
vol: 12,
page: 512,
stat: Journal Article,
PLASMA-RENIN AND SERUM DOPAMINE-BETA-HYDROXYLASE DURING ORTHOSTATIC HYPOTENSION IN QUADRIPLEGIC MAN
KAMELHAR, DL; STEELE, JM; SCHACHT, RG; LOWENSTEIN, J; SELL, GH; NAFTCHI, NE
1977 ;58(11):534-534, Archives of physical medicine & rehabilitation
—
id: 39915,
year: 1977,
vol: 58,
page: 534,
stat: Journal Article,
Failure of sodium restriction to abolish exaggerated natriuresis in poststreptococcal glomerulonephritis
Schacht RG; Steele JM Jr; Lowenstein J; Baldwin DS
1977 ;18(6):333-341, Nephron
Exaggerated natriuresis in response to hypertonic saline infusion occurs with great regularity in patients with documented previous attacks of poststreptococcal glomerulonephritis. Five patients were studied before and after 1 week of dietary sodium restriction in order to examine the possibility that increased extracellular fluid volume might play a role in the response to acute saline infusion. Plasma renin activity (PRA) and PRA responsiveness to sodium depletion were normal, suggesting that extracellular fluid volume was not increased. In all patients, extracellular fluid volume decreased during sodium restriction, as judged by weight loss, cumulative negative sodium balance, small decreases in measured plasma volume, and appropriate increases of PRA and plasma aldosterone concentration. Hypertonic saline infusion provoked exaggerated natriuresis in all patients equally as well after dietary sodium restriction as before. Exaggerated natriuresis in poststreptococcal glomerulonephritis occurs without evidence of chronic expansion of extracellular fluid volume and is not affected by reduction of extracellular fluid volume
—
id: 65188,
year: 1977,
vol: 18,
page: 333,
stat: Journal Article,
FAILURE OF KIDNEY TO VASODILATE DURING DOPAMINE INFUSION IN DIABETES-MELLITUS
Schacht, RG; Baldwin, DS
1977 ;12(6):474-474, Kidney international
—
id: 29961,
year: 1977,
vol: 12,
page: 474,
stat: Journal Article,
ACUTE RENAL-INSUFFICIENCY (ARI) FOLLOWING OPEN-HEART SURGERY (OHS)
Schacht, RG; Eagan, P; Doyle, EF
1977 ;11(4):400-400, Pediatric research
—
id: 29611,
year: 1977,
vol: 11,
page: 400,
stat: Journal Article,
COURSE OF POSTSTREPTOCOCCAL GLOMERULONEPHRITIS - REPLY
SCHACHT, RG; GLUCK, MC; GALLO, GR; BALDWIN, DS
1977 ;296(4):231-231, New England journal of medicine
—
id: 40026,
year: 1977,
vol: 296,
page: 231,
stat: Journal Article,
EXAGGERATED VASOCONSTRICTOR RESPONSE IN POSTSTREPTOCOCCAL GLOMERULONEPHRITIS(PSGN)
Schacht, RG; Iqbal, MS; Baldwin, DS
1977 ;25(3):A508-A508, Clinical research
—
id: 29601,
year: 1977,
vol: 25,
page: A508,
stat: Journal Article,
PRESSURE NATRIURESIS IN EXPERIMENTAL GLOMERULO NEPHRITIS
Schacht, RG; Iqbal, MS; Schulman, G; Baldwin, DS
1977 ;11(4):557-557, Pediatric research
—
id: 29617,
year: 1977,
vol: 11,
page: 557,
stat: Journal Article,
Chyluria in an adolescent hemophiliac. A discussion of diagnosis and management
Schneider, J; Schacht, R G
1977 Oct;16(10):959-960, Clinical pediatrics
—
id: 150009,
year: 1977,
vol: 16,
page: 959,
stat: Journal Article,
Late sequelae of poststreptococcal glomerulonephritis
Baldwin DS; Schacht RG
1976 ;27:49-55, Annual review of medicine
—
id: 65191,
year: 1976,
vol: 27,
page: 49,
stat: Journal Article,
SERUM DOPAMINE-BETA-HYDROXYLASE AND PLASMA-RENIN ACTIVITIES DURING TILTING IN QUADRIPLEGIA
Kamelhar, DL; Steele, JM; Schacht, RG; Lowenstein, J; Naftchi, NE
1976 ;24(3):A224-A224, Clinical research
—
id: 28750,
year: 1976,
vol: 24,
page: A224,
stat: Journal Article,
Progression to uremia after remission of acute poststreptococcal glomerulonephritis
Schacht RG; Gluck MC; Gallo GR; Baldwin DS
1976 Oct 28;295(18):977-981, New England journal of medicine
Whether or not poststreptococcal glomerulonephritis advances over the long term to uremia remains an unsettled issue. We documented ultimate progression to renal failure in six patients who were observed at onset with the typical clinical and morphologic features of acute nephritis after proved beta-hemolytic streptococcal infection. Within one year, renal function returned essentially to normal in all, as the proliferative changes in glomeruli subsided, Subsequently, increasing renal failure developed in these patients over periods ranging from two to 12 years, during which all were hypertensive. As the renal disease progressed, glomeruli showed increasing sclerosis in the absence of proliferation, and fibrohyaline thickening of renal arterioles appeared
—
id: 59979,
year: 1976,
vol: 295,
page: 977,
stat: Journal Article,
EXAGGERATED VASOCONSTRICTOR RESPONSE IN POSTSTREPTOCOCCAL GLOMERULONEPHRITIS(PSGN)
Schacht, RG; Iqbal, MS; Baldwin, DS
1976 ;10(6):565-565, Kidney international
—
id: 29647,
year: 1976,
vol: 10,
page: 565,
stat: Journal Article,
PRESSURE NATRIURESIS IN EXPERIMENTAL GLOMERULONEPHRITIS
Schacht, RG; Iqbal, MS; Schulman, G; Baldwin, DS
1976 ;24(3):A411-A411, Clinical research
—
id: 29464,
year: 1976,
vol: 24,
page: A411,
stat: Journal Article,
PRESSURE NATRIURESIS - IN EXPERIMENTAL GLOMERULONEPHRITIS
Schulman, G; Schacht, RG; Iqbal, MS; Baldwin, DS
1976 ;10(6):565-565, Kidney international
—
id: 29648,
year: 1976,
vol: 10,
page: 565,
stat: Journal Article,
Unilateral renal vein thrombosis during mid-childhood
Florman, A L; Schacht, R G; Becker, M H; Genieser, N B; Madayag, M A
1975 Aug;14(8):734-7 passium, Clinical pediatrics
—
id: 106553,
year: 1975,
vol: 14,
page: 734,
stat: Journal Article,
PROGRESSION TO UREMIA AFTER SUBSIDENCE OF ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS (PSGN)
Schacht, RG; Gluck, MC; Gallo, G; Baldwin, DS
1975 ;8(6):419-419, Kidney international
—
id: 29507,
year: 1975,
vol: 8,
page: 419,
stat: Journal Article,
LONG-TERM FOLLOW-UP OF POSTSTREPTOCOCCAL GLOMERULONEPHRITIS IN CHILDREN
Schacht, RG; Iqbal, MS; Baldwin, DS
1975 ;9(4):379-379, Pediatric research
—
id: 28571,
year: 1975,
vol: 9,
page: 379,
stat: Journal Article,
LONG-TERM COURSE OF POSTSTREPTOCOCCAL GLOMERULONEPHRITIS IN CHILDREN
Schacht, RG; Iqbal, MS; Gluck, MC; Gallo, G; Baldwin, DS
1975 ;23(3):A373-A373, Clinical research
—
id: 28540,
year: 1975,
vol: 23,
page: A373,
stat: Journal Article,
The long-term course of poststreptococcal glomerulonephritis
Baldwin DS; Gluck MC; Schacht RG; Gallo G
1974 Mar;80(3):342-358, Annals of internal medicine
—
id: 65168,
year: 1974,
vol: 80,
page: 342,
stat: Journal Article,
INFANTILE RICKETS WITH SEVERE PROXIMAL RENAL TUBULAR-ACIDOSIS, RESPONSIVE TO VITAMIN-D
HUGUENIN, M; SCHACHT, R; DAVID, R
1974 ;49(12):955-959, Archives of disease in childhood
—
id: 48867,
year: 1974,
vol: 49,
page: 955,
stat: Journal Article,
Exaggerated natriuresis in the course of poststreptococcal glomerulonephritis
Schacht RG; Steele JM Jr; Baldwin DS
1974 ;13(5):349-364, Nephron
—
id: 65166,
year: 1974,
vol: 13,
page: 349,
stat: Journal Article,
Long-term follow-up of poststreptococcal glomerulonephritis
Baldwin DS; Gluck MC; Schacht RG; Moussalli A; Gallo GR
1973 ;1 Pt 1:327-343, Perspectives in nephrology & hypertension
—
id: 59982,
year: 1973,
vol: 1 Pt 1,
page: 327,
stat: Journal Article,
EXAGGERATED NATRIURESIS IN COURSE OF POSTSTREPTOCOCCAL GLOMERULONEPHRITIS
SCHACHT, RG; STEELE, JM; BALDWIN, DS
1973 ;7(4):416-416, Pediatric research
—
id: 39795,
year: 1973,
vol: 7,
page: 416,
stat: Journal Article,
Renal mechanism for DOCA escape in man
Schacht, R G; Lowenstein, J; Baldwin, D S
1971 Oct;47(10):1233-1233, Bulletin of the New York Academy of Medicine
—
id: 65170,
year: 1971,
vol: 47,
page: 1233,
stat: Journal Article,


