Anthropometric Renal Anatomic Alterations Between Supine and Prone Positions in Percutaneous Renal Ablation for Renal Cortical Neoplasms

Context While biopsies are now increasingly being performed for the diagnosis of renal cortical neoplasms, the influence of the rendered pathological diagnoses on the clinical management is only rarely documented. Objectives To report our experience with consecutively performed renal biopsies and the potential impact of the diagnosis on subsequent clinical management. Design Material from needle biopsies performed consecutively at our institution between 2006 and 2011 was reviewed. The influence of the reported pathology results on the clinical management was determined from patient follow-up medical record review. Results In total, 218 percutaneous biopsies for renal masses were performed during this period. Among them, 181 (83%) yielded neoplastic tissue, including 81 clear cell renal cell carcinomas, 29 low-grade oncocytic neoplasms, 7 papillary renal cell carcinomas, 5 clear cell papillary renal cell carcinomas, 5 angiomyolipomas, and 14 urothelial carcinomas. Fourteen additional cases (6%) contained lesional material from clinically known nonneoplastic processes, for a total diagnostic yield of 89%. Twenty-three (11%) were nonrepresentative of lesional tissue. In 10 of these, repeat biopsies or resections established the diagnosis of renal tumors. Biopsy diagnosis was confirmed in 29 of 30 cases (97%) on subsequent nephrectomy. Following the biopsy diagnosis, there were significant differences in the clinical management; overall, 79% of clear cell renal cell carcinomas received therapeutic interventions, and 17% were put on active surveillance. In contrast, 77% of the benign or low-grade lesions were put on active surveillance. Conclusions Accurate and specific diagnosis can be rendered on renal core biopsy in most renal tumors, and the biopsy diagnosis can have a definitive role in their clinical management.

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ELECTROPHORETIC EVIDENCE FOR ISOZYMES OF ARYLAMIDASE ("AMINOPEPTIDASE") IN THE RAT. I. RENAL, SERUM AND URINARY ENZYMES SPLITTING dl-ALANYL-2-NAPHTHYLAMIDE AND l-LEUCYL-2-NAPHTHYLAMIDE

Journal of Histochemistry & Cytochemistry ◽

10.1177/12.12.869 ◽

1964 ◽

Vol 12 (12) ◽

pp. 869-874 ◽

Cited By ~ 11

Author(s):

BENITO MONIS

Keyword(s):

Present Report ◽

Molecular Forms ◽

Supernatant Fraction ◽

Blood Levels ◽

Rat Tissues ◽

Bilateral Nephrectomy ◽

Rat Urine ◽

Urinary Enzyme ◽

Renal Ablation ◽

Starting Point

Bilateral nephrectomy elicited no changes of serum blood levels of arylamidase assayed with two chromogenic substrates (l-leucyl-2-naphthylamide and dl-alanyl-2-naphthylamide) two days after the operation. Since rat urine contains similar enzymes it was postulated that the urinary enzyme is of renal origin and distinct from serum arylamidase. For this purpose, electrophoretic studies were undertaken. Starch block (for quantitative determinations) and starch gel for zymograms of arylamidase were used. It was shown that both procedures demonstrated the identity of urinary and renal arylamidase, which was distinct from the serum enzyme. The renal and urinary enzyme showed two distinct isozymes: one remaining at the origin and the other migrating somewhat less than the isozyme in serum. It is postulated that the isozyme remaining at the origin corresponds to a membrane-bound form, whereas the electrophoretically-mobile isozyme is found in the cellular supernatant fraction. The arylamidase from serum was represented by a single enzyme which migrated farthest towards the anode. Histochemical procedures for the demonstration of arylamidase activity in tissues at the light microscopic level permit the localization of enzyme(s) that can hydrolyze synthetic chromogenic naphthylamides containing l-leucyl and dl-alanyl groups (1). Rat kidneys have a high concentration of histochemically demonstrable arylamidase in the proximal convoluted tubules (2). Blood levels of arylamidase in the normal adult rat vary within a narrow range (3). The observation of arylamidase activity in rat urine raised several questions that led to the studies which are the basis of the present report. The relationship of serum and urinary arylamidase was the starting point of this investigation. It was speculated that if the urinary enzyme had its origin in the serum, bilateral nephrectomy should alter blood levels of the enzyme. If no such changes occurred, this would suggest that the urinary enzyme was released from the proximal convoluted tubule. In fact, total renal ablation led to no significant variation of serum arylamidase activity. It was therefore postulated that urinary arylamidase originated in the kidneys and that both are distinct from serum arylamidase. To test this hypothesis, zone electrophoretic studies were undertaken using two different supporting media. It will be shown that distinct molecular forms or isozymes of arylamidase can be separated from rat tissues and fluids by differential electrophoretic mobility. The electrophoretic identity of urinary and renal arylamidase, both of which are distinct from the serum arylamidase, is demonstrated in this study.

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PCR-Based RFLP Screening of the Commonly Deleted 3p Loci in Renal Cortical Neoplasms

Diagnostic Molecular Pathology ◽

10.1097/00019606-199312000-00007 ◽

1993 ◽

Vol 2 (1) ◽

pp. 269-276 ◽

Cited By ~ 14

Author(s):

Adel K. El-Naggar ◽

John G. Batsakis ◽

Gang Wang ◽

Ming-Sheng Lee

Keyword(s):

Renal Cortical Neoplasms

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In vivo renal arginine release is impaired throughout development of chronic kidney disease

AJP Renal Physiology ◽

10.1152/ajprenal.00487.2009 ◽

2010 ◽

Vol 298 (1) ◽

pp. F95-F102 ◽

Cited By ~ 20

Author(s):

Gin-Fu Chen ◽

Chris Baylis

Keyword(s):

Chronic Kidney Disease ◽

Kidney Disease ◽

Renal Plasma Flow ◽

Severe Injury ◽

Normal Kidney ◽

Plasma Citrulline ◽

Renal Ablation ◽

Early Injury ◽

Production Increase

The kidney is a major site of arginine synthesis where citrulline is converted to arginine via argininosuccinate synthase (ASS) and lyase (ASL). The rate-limiting step in arginine synthesis by the normal kidney is the rate of citrulline delivery and uptake to the renal cortex. We tested whether with chronic kidney disease (CKD) renal arginine synthesis may be compromised. Using the renal ablation/infarction (A/I) injury model, we measured renal citrulline delivery and uptake as well as arginine release at early, moderate, and severe stages of CKD vs. healthy controls. The renal plasma flow (RPF) and arterial-renal venous difference was measured at baseline and during citrulline infusion. Citrulline delivery was reduced at all stages of disease due to marked reductions in RPF and despite moderately increased plasma citrulline. Early after A/I, the kidney demonstrated a compensatory increase in citrulline uptake while at moderate and severe injury baseline citrulline uptake fell. At all stages of CKD, renal arginine release was markedly reduced. Citrulline infusion increased plasma citrulline in all groups, resulting in increased renal delivery vs. baseline. In healthy kidneys and early injury, citrulline uptake increased with the infusion, but only in the normal kidney did arginine production increase in parallel with the increased citrulline uptake. At moderate and severe injury, there was no increase in citrulline uptake or arginine production. The fall in arginine production in A/I was due to an early loss of ASS and ASL conversion of citrulline, which combined with a later reduction in citrulline uptake.

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