Combination of Exercise and Enalapril Enhances Renoprotective and Peripheral Effects in Rats With Renal Ablation

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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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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Imaging following renal ablation: what can we learn from recurrent tumors?

Abdominal Radiology ◽

10.1007/s00261-018-1541-0 ◽

2018 ◽

Vol 43 (10) ◽

pp. 2750-2755 ◽

Cited By ~ 5

Author(s):

Patrick W. Eiken ◽

Thomas D. Atwell ◽

A. Nicholas Kurup ◽

Stephen A. Boorjian ◽

R. Houston Thompson ◽

...

Keyword(s):

Recurrent Tumors ◽

Renal Ablation

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Glucocorticoids Amplify Glomerular Injury in Rats with Renal Ablation

American Journal of Hypertension ◽

10.1093/ajh/1.1.54 ◽

1988 ◽

Vol 1 (1) ◽

pp. 54-57 ◽

Cited By ~ 2

Author(s):

Diego L. García ◽

Helmut G. Rennke ◽

Barry M. Brenner ◽

Sharon Anderson

Keyword(s):

Glomerular Injury ◽

Renal Ablation

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Abstract 153: Born with a Single Kidney versus Nephrectomy: Similar End Point, Different Mechanism of Injury

Hypertension ◽

10.1161/hyp.60.suppl_1.a153 ◽

2012 ◽

Vol 60 (suppl_1) ◽

Author(s):

Xuexiang Wang ◽

Ashley Johnson ◽

Jonathan Lee ◽

Leah Solberg-Woods ◽

Michael R Garrett

Keyword(s):

Renal Function ◽

Renal Injury ◽

Time Course ◽

Course Evaluation ◽

Pathophysiological Mechanism ◽

Mechanism Of Injury ◽

Nephron Number ◽

Unilateral Renal Agenesis ◽

Renal Ablation ◽

Single Kidney

A relatively common abnormality of the urogenital tract in humans is the development of only a single kidney (1:500 to 1:1000). Clinical studies suggest that patients born with a single kidney can develop proteinuria, hypertension, and even renal failure later in life. In contrast, studies in children who undergo nephrectomy or adults who serve as kidney donors appear to exhibit little difference in renal function compared to two-kidney subjects. Invasive techniques such as nephrectomy or renal ablation have been used to generate animal models to recapitulate this human congenital disorder. The progression of injury in these models is attributed to hyperfiltration which refers to changes in hemodynamics that cause glomerular damage leading to hypertension. Recently, our lab developed a new genetic animal model [heterogeneous stock derived model of unilateral renal agenesis, (HSRA)] that develops with a single kidney in 50-75% of offspring. The model is characterized by reduced nephron number, kidney hypertrophy, and renal injury that leads to a decline in renal function. Time course evaluation of blood pressure, renal hemodynamics, and renal injury was performed in 4 groups; (1) HSRA-S (1-kidney), (2) HSRA-C (2-kidney littermates), (3) HSRA-UNX3 (uninephrectomy-week 3) and (4) HSRA-UNX8 (uninephrectomy-week 8). Nephrectomized animals demonstrated hyperfiltration, whereas single kidney animals (HSRA-S) did not. This suggests a different pathophysiological mechanism of injury between congenital and nephrectomized rats. At later time points, proteinuria for HSRA-UNX3 (82±22.9 mg/24h) and HSRA-UNX8 (46±18.1) were significantly higher than HSRA-C (11±6.4), while HSRA-S (109±15.7) demonstrated the highest proteinuria. GFR was lowest in HSRA-S (656±123.9 ul/min/gKW), followed by HSRA-UNX3 (1151±112.4), HSRA-UNX8 (1309±98.3) and HSRA-C (1544±111.7). Microarray studies have identified several developmental genes ( Hox5b , Smoc2 and c- Kit ) that may be linked to reduced nephron number and other structural changes that could predispose the HSRA-S to kidney injury later in life. These results demonstrate that rats born with a single kidney are more prone to renal injury than nephrectomized rats and the mechanism is likely different.

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