scholarly journals THE DEGREE OF COMPENSATORY RENAL HYPERTROPHY FOLLOWING UNILATERAL NEPHRECTOMY

1932 ◽  
Vol 56 (2) ◽  
pp. 255-265 ◽  
Author(s):  
E. M. MacKay ◽  
L. L. MacKay ◽  
T. Addis
Keyword(s):  
Adult Life ◽  
Compensatory Hypertrophy ◽  
Rapid Decrease ◽  
Unilateral Nephrectomy ◽  
Albino Rats ◽  
Renal Hypertrophy ◽  
Compensatory Renal Hypertrophy

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.

scholarly journals THE DEGREE OF COMPENSATORY RENAL HYPERTROPHY FOLLOWING UNILATERAL NEPHRECTOMY

1938 ◽  
Vol 67 (4) ◽  
pp. 515-519 ◽  
Author(s):  
Lois L. MacKay ◽  
T. Addis ◽  
Eaton M. MacKay
Keyword(s):  
Protein Intake ◽  
Compensatory Hypertrophy ◽  
Unilateral Nephrectomy ◽  
Albino Rats ◽  
Renal Hypertrophy ◽  
Young Rats ◽  
Compensatory Renal Hypertrophy ◽  
Old Rats

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.

Endothelial dysfunction promotes the transition from compensatory renal hypertrophy to kidney injury after unilateral nephrectomy in mice

2012 ◽  
Vol 302 (11) ◽  
pp. F1402-F1408 ◽  
Author(s):  
Hajime Nagasu ◽  
Minoru Satoh ◽  
Kengo Kidokoro ◽  
Yuko Nishi ◽  
Keith M. Channon ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Soluble Guanylate Cyclase ◽  
Kidney Injury ◽  
Compensatory Hypertrophy ◽  
Initiation Factor ◽  
Unilateral Nephrectomy ◽  
Wild Type ◽  
Renal Hypertrophy ◽  
No Donor ◽  
Compensatory Renal Hypertrophy

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.

scholarly journals Conservation of ribosomal RNA during compensatory renal hypertrophy. A major mechanism in RNA accretion.

1976 ◽  
Vol 69 (3) ◽  
pp. 548-556 ◽  
Author(s):  
W T Melvin ◽  
A Kumar ◽  
R A Malt
Keyword(s):  
Ribosomal Rna ◽  
Cultured Cells ◽  
Compensatory Hypertrophy ◽  
Mouse Kidney ◽  
Average Increase ◽  
Renal Hypertrophy ◽  
Major Mechanism ◽  
Compensatory Renal Hypertrophy

After removal of one mouse kidney, compensatory hypertrophy in the remaining kidney is marked in 2 days by a 20% average increase in ribosomal RNA (rRNA) per cell. Both 28S and 18S RNA are conserved during the initial stages of compensatory renal hypertrophy to an extent sufficient to account for the rest of the observed accumulation of rRNA. Like some cultured cells, the kidney conserves rRNA during physiological growth.

scholarly journals Nitric Oxide in Serum and Renal Tissue During Compensatory Renal Hypertrophy in Rats

2006 ◽  
Vol 6 (1) ◽  
pp. 46-49 ◽  
Author(s):  
Jasminko Huskić ◽  
Asija Začiragić ◽  
Nermina Babić ◽  
Nedžad Mulabegović
Keyword(s):  
Nitric Oxide ◽  
Renal Tissue ◽  
Unilateral Nephrectomy ◽  
Hemodynamic Changes ◽  
Renal Hypertrophy ◽  
Griess Reaction ◽  
Reaction Conversion ◽  
Compensatory Renal Hypertrophy ◽  
Male Wistar Rats ◽  
Dorsolateral Approach

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.

Compensatory renal hypertrophy. I. Evidence for a factor of renal origin inhibiting DNA synthesis

1977 ◽  
Vol 55 (4) ◽  
pp. 839-847 ◽  
Author(s):  
J. Martel-Pelletier ◽  
M. Bergeron
Keyword(s):  
Molecular Weight ◽  
Dna Synthesis ◽  
Specific Inhibitor ◽  
Inhibitory Effect ◽  
Compensatory Hypertrophy ◽  
Partial Purification ◽  
Dna Uptake ◽  
Renal Hypertrophy ◽  
Compensatory Renal Hypertrophy

This study describes a method for the measurement and partial purification of a factor seemingly involved in the regulation of the renal mass.After homogenization at 4 °C, rabbit kidneys were centrifuged for 100 min at 105 000 g. The resulting supernatant (S-105) was lyophilized and tested on kidney slices obtained from rats mononephrectomized 48 h previously. We have developed a method based on the inhibition of DNA synthesis to measure the activity of the S-105. Slices of renal cortex, undergoing compensatory hypertrophy, were incubated in vitro in Hanks' medium at 37 °C, pH 7.4, in an O2–CO2 atmosphere in the presence of 0.144 μg (20 μCi (1 Ci = 37 GBq)) [3H]thymidine.An inhibition of DNA uptake of [3H]thymidine was noted in the presence of S-105. When other media (Hanks', sucrose, water) were used to extract S-105, the same type of inhibition was noted even though the sucrose buffer seemed ideal for the preservation of the inhibitory factor. The inhibitory effect was still observed after dialysis of S-105 against membranes permitting exclusion of molecules with molecular weight smaller than about 4000 (such as electrolytes and tissue thymidine). This inhibition seems to be specific, since other tissues such as liver in regeneration and rat intestine were not influenced by the dialyzed renal S-105. The dialyzable fraction did contain some inhibitors, but they were not specific for the kidney since they also acted on the liver and the jejunum.Our results suggest the existence, in the normal nephron, of a specific inhibitor of thymidine incorporation into DNA of kidneys undergoing a compensatory hypertrophy. This renal factor has a molecular weight of over 5000.

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