On Compensatory Renal Hypertrophy After Unilateral Nephrectomy

1957 ◽  
Vol 41 (1) ◽  
pp. 34-43 ◽  
Author(s):  
Carl-Martin Fajers
1938 ◽  
Vol 67 (4) ◽  
pp. 515-519 ◽  
Author(s):  
Lois L. MacKay ◽  
T. Addis ◽  
Eaton M. MacKay

Compensatory hypertrophy of the kidney in albino rats is increased by an increase in the protein intake. The effect is greater in old rats than young rats. Successive increases in the protein intake are followed by a reduction in the increase in the degree of compensatory renal hypertrophy.


2006 ◽  
Vol 6 (1) ◽  
pp. 46-49 ◽  
Author(s):  
Jasminko Huskić ◽  
Asija Začiragić ◽  
Nermina Babić ◽  
Nedžad Mulabegović

Nitric oxide (NO) level in serum and renal tissue has been examined in 15 male Wistar rats, body weight 200-250 g, 7 days after unilateral nephrectomy. All rats were ether-anaesthetized and the kidneys were removed by dorsolateral approach. NO concentration in serum and renal tissue was determined by classic colorimetric Griess reaction. Conversion of NO(3)(2-) into NO(2)(2-) was done with elementary zinc. Results have shown that NO concentration in renal tissue is statistically higher in rats 7 days after unilateral nephrectomy then in control renal tissue before compensatory kidney growth (p<0,02). There is no difference between NO concentration in serum before unilateral nephrectomy and 7 days after nephrectomy. These findings suggest that NO may play an important role in mediating the hemodynamic changes associated with reduced renal mass.


2012 ◽  
Vol 302 (11) ◽  
pp. F1402-F1408 ◽  
Author(s):  
Hajime Nagasu ◽  
Minoru Satoh ◽  
Kengo Kidokoro ◽  
Yuko Nishi ◽  
Keith M. Channon ◽  
...  

Loss of functional nephrons associated with chronic kidney disease induces glomerular hyperfiltration and compensatory renal hypertrophy. We hypothesized that the endothelial nitric oxide synthase (eNOS) [soluble guanylate cyclase (sGC)] protein kinase G (PKG) pathway plays an important role in compensatory renal hypertrophy after unilateral nephrectomy. Analysis of mice subjected to unilateral nephrectomy showed increases in kidney weight-to-body weight and total protein-to-DNA ratios in wild-type but not eNOS knockout (eNOSKO) mice. Serum creatinine and blood urea nitrogen increased after nephrectomy in eNOSKO but not in wild-type mice. Furthermore, Bay 41–2272, an sGC stimulator, induced compensatory renal hypertrophy in eNOSKO mice and rescued renal function. The NO donor S-nitrosoglutathione (GSNO) and Bay 41–2272 stimulated PKG activity and induced phosphorylation of Akt protein in human proximal tubular cells. GSNO also induced phosphorylation of eukaryotic initiation factor 4E-binding protein and ribosomal protein S6. Our results highlight the importance of the eNOS-NO-PKG pathway in compensatory renal hypertrophy and suggest that reduced eNOS-NO bioavailability due to endothelial dysfunction is the underlying mechanism of failure of compensatory hypertrophy and acceleration of progressive renal dysfunction.


1932 ◽  
Vol 56 (2) ◽  
pp. 255-265 ◽  
Author(s):  
E. M. MacKay ◽  
L. L. MacKay ◽  
T. Addis

Compensatory hypertrophy of the kidney in albino rats becomes less as age advances. There is a rapid decrease from 5 days to 60 days of age and then a slow diminution throughout adult life.


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