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The American Journal of Medicine | 1978

Acute renal failure following drip infusion pyelography

Alejandro Carvallo; Thomas A. Rakowski; William P. Argy; George E. Schreiner

Abstract Acute renal failure is a well-known complication of intravenous pyelography in patients with diabetes mellitus or multiple myeloma. We describe 10 patients in whom acute renal failure developed after drip infusion pyelography (DIP). Of these patients, only four were diabetic and none had multiple myeloma. All patients had preexisting renal disease. Serum creatinine was higher than 1.5 mg/dl in eight. Proteinuria, vascular disease, dehydration and fluid overload were all seen in the group. An increase in serum creatinine was noted in all patients within 48 hours following DIP. Urine volume decreased in eight patients within 24 hours after the examination. Renal function returned to the levels pre-DIP in three patients in periods ranging from eight to 10 days. In five others, serum creatinine decreased almost to the prestudy levels but remained elevated by 0.7 to 1.4 mg/dl at the time of the last observation. No patient died of acute renal failure. The data indicate that (1) preexisting renal insufficiency in the setting of systemic disease is the most prevalent predisposing factor to acute renal failure after DIP; (2) renal hypoperfusion of various types seemed to render these patients susceptible to acute renal failure after DIP; (3) in some patients, acute renal failure was not typical of acute tubular necrosis; and (4) recovery of renal function toward base line after a short period of oliguria frequently occurred. In 10 patients acute renal failure developed after drip infusion pyelography (DIP). Six had neither diabetes mellitus nor multiple myeloma. All patients had preexisting renal disease. Proteinuria, vascular disease, fluid overload and volume contraction were noted. All patients had elevated serum creatinine levels and eight were oliguric. Return of renal function toward base line was frequently seen. The prevalent predisposing cause of acute renal failure after DIP was preexisting renal disease on a background of systemic disease.


Nephron | 1976

Evaluation of Percutaneous Kidney Biopsy in Advanced Renal Failure

John J. Curtis; Thomas A. Rakowski; William P. Argy; George E. Schreiner

As more information is gained on the long-term survival in chronic dialysis and transplant patients, it is unacceptable to be satisfied with a clinical impression of the etiology of the end stage renal failure in each case. It becomes important to know the histological diagnosis in patients who present with terminal renal failure. In the past there was little to offer such individuals in terms of therapeutics, and their prognosis was uniformly poor. Thus, biopsy for other than academic reasons was difficult to justify. This is no longer true and presented here is a series of 28 such patients in whom percutaneous renal biopsy was performed. The complications and diagnostic yield are reported. It is further demonstrated that the added knowledge of histological diagnosis can be of benefit to the individual patient.


American Journal of Kidney Diseases | 2008

BK Virus–Associated Nephropathy in a Patient With AIDS

William R. Sukov; Matthew Lewin; Sanjeev Sethi; Thomas A. Rakowski; Donna J. Lager

The BK virus is a ubiquitous member of the group of human polyoma viruses that commonly is reactivated in the setting of immunosuppression related to renal transplantation, which results in tubulointerstitial nephritis and allograft dysfunction. BK virus-associated nephropathy occurring in association with human immunodeficiency virus infection and acquired immunodeficiency syndrome (AIDS) was reported only rarely. We describe the case of a 43-year-old man with AIDS presenting with nonoliguric renal failure. The renal biopsy specimen showed tubulointerstitial nephritis and renal tubular cell changes consistent with BK viral inclusions. Results of in situ hybridization for BK viral DNA were positive and showed tubular cell intranuclear inclusions. To our knowledge, this represents the third case of AIDS-associated BK virus-associated nephropathy diagnosed by means of biopsy.


Nephron | 1990

Effect of urine osmolality on urinary red cell morphology.

Stephen N. Turitzin; Carlos Rotellar; James F. Winchester; Robert C. Mackow; Thomas A. Rakowski; John J. Pahira

Stephen N. Turitzin, MD, Georgetown University, Medical Center, Nephrology Division, 3800 Reservoir Road, Washington, DC 20007 (USA) Dear Sir, We have read with interest the article by De Caes-tecker et al. [1] on the localization of hematuria by red cell analyzers and phase contrast microscopy. We disagree with their conclusion that urine osmolality does not affect the urinary erythrocyte cell size distribution. Although this may be true for situations in which high urine osmolality is encountered, it is not the case for hypotonic urine. As part of a larger study of urinary red cell morphology following extracorporeal shock wave lithotripsy [2], we examined erythrocyte size distributions in mixtures of blood and urine of different tonicities. We found that low urine osmolality substantially altered red cell size determined by cell counter. Urine collected from a healthy male volunteer was diluted with varying proportions of distilled water to produce samples with a range of osmolalities from 68 to 758 mosm/kg. One hundred microliters of whole blood was mixed with 10 ml of each of these urine samples. After 30–60 min incubation, 50 μl of each mixture were added to 25 ml of isotonic buffer for determination of cell size distributions and median cell volume using a cell counter (Electrozone/Celloscope Model 112 CLT, Ill.). Cell counts were made before and after addition of a lysing agent (Zapoglobinll, Coulter Electronics, Fla.) to eliminate counts due to nonerythrocyte debris. We found that above 210 mosm/kg osmolality had little effect on red cell size, but that below this value median cell volume fell. Figure 1 shows red cell size distributions in urine samples with osmolalities of 89, 140, and 247 mosm/kg. The mean median cell volume in eight urine samples with osmolalities between 68 and 201 • · 89 mOsm/Kg * a 140 mOsm/Kg ■ ■ 247 mOsm/Kg Fig. 1. Cell size frequency distributions of erythrocytes incubated in urines of three different osmolalities. mosm/kg was 46.6 ± 14.2 fl (mean ± SD), while the mean median red cell volume in ten urine samples with osmolalities between 228 and 758 mosm/kg was 101.1 ± 9.5 fl. This difference was


Archive | 1986

Creatine Kinase, Amylase, and Parathyroid Hormone in Stable CAPD and Hemodialysis Patients

J. Rahmat; J. F. McAnally; James F. Winchester; Thomas A. Rakowski; N. Perri; William P. Argy; George E. Schreiner

Since there are conflicting reports on elevation of plasma creatine kinase and amylase above normal in dialysis patients we studied total and isoenzyme fractions of creatine kinase and amylase. In addition since hyperparathyroidism and pancreatitis are associated we also studied plasma-n-terminal parathyroid hormone levels. Studies were performed in 35 stable CAPD patients, and creatine kinase alone was studied in 11 stable hemodialysis patients. Total creatine kinase was elevated in nine of 35 CAPD patients (25.7%); elevated isoenzyme fractions of CK were as follows: nine of nine patients had elevated MM band, one of nine had elevated MB and one of nine had elevated BB band. In the hemodialysis patients two of 11 had elevated CK (MM bands). Total amylase was elevated in 17 of 26 CAPD patients with ten of these patients having an elevated pancreatic isoenzyme fraction; in six of 17, the salivary isoenzyme fraction equalled the pancreatic enzyme fraction in one patient. Parathyroid hormone was elevated in 24 of 35 CAPD patients, but no correlation existed between parathyroid hormone levels, creatine kinase and amylase, although there was a significant correlation between creatine kinase and amylase levels in CAPD patients (r = 0.4, n = 23, p < 0.05). These findings suggest a common etiology for elevated creatine and amylase in otherwise stable CAPD patients such as inadequate dialysis, subclinical skeletal myopathy, or metabolic complications. These findings warrant further study.


Nephron | 1977

Effects of Metabolic Acidosis on Renal Na and H2O Handling in Humans

L.L. Vertuno; Thomas A. Rakowski; E. McCarthy; Harry G. Preuss

An acidotic state has been shown to inhibit sodium (Na) transport both in vitro in toad and turtle bladders an in vivo in rat and dog proximal tubules. To determine if renal Na transport was altered i


Archive | 1986

The Telephone—An Underestimated Resource for CAPD Nursing Management

W. F. Barnard; N. Kloberdanz; William P. Argy; Thomas A. Rakowski; James F. Winchester

Telephone communication between CAPD nursing staff and patients, avoids unnecessary delays in dealing with simple problems, giving support to patients, and judging whether patients have serious problems necessitating acute nursing/medical management. The telephone serves as a vital link between patient and nursing personnel.


Annals of Internal Medicine | 1982

Survival with End-Stage Renal Disease

Alexander C. Chester; William P. Argy; Thomas A. Rakowski; George E. Schreiner

Excerpt To the editor: Hutchinson and associates (1) make a substantial contribution to the type of analysis needed to understand the natural history of end-stage renal disease. Data such as these ...


Cellular and Molecular Life Sciences | 1978

A lack of correlation between rat kidney mitochondrial swelling and glutaminase activation in metabolic acidosis

Thomas A. Rakowski; L.L. Vertuno; Harry G. Preuss

We found no overall correlation between mitochondrial swelling and PDG activity under many different conditions. We conclude that augmented PDG activity in acidosis is not related, at least to any great extent, to increased anion permeability produced by mitochondrial swelling.


JAMA Internal Medicine | 1979

Hemodialysis in the eighth and ninth decades of life.

Alexander C. Chester; Thomas A. Rakowski; William P. Argy; Anna Giacalone; George E. Schreiner

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Carlos Rotellar

Georgetown University Medical Center

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