scholarly journals Remnant kidney metabolism in the dog.

1991 ◽  
Vol 2 (1) ◽  
pp. 70-76
Author(s):  
A Fine
Keyword(s):  
Glomerular Filtration Rate ◽  
Metabolic Acidosis ◽  
Oxygen Uptake ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Normal Kidney ◽  
Renal Metabolism ◽  
Energy Substrates ◽  
Chronic Metabolic Acidosis ◽  
Remnant Kidney

A marked increase in oxygen uptake (Qo2) per nephron has been described in the remnant kidney of the rat. However, it is not known which substrates support renal metabolism in remnant kidney nor is it known whether similar changes in Qo2 occur in other species. Remnant kidney in the dog was induced by ligation of 60 to 75% of the renal arterial branches on one side followed 1 to 2 wk later by contralateral nephrectomy. At 3 months marked hypertrophy of the remnant kidney was found and the glomerular filtration rate was 18 +/- 1.8 mL/min compared with 31 +/- 2 in a normal kidney (P less than 0.01). Qo2 was 689 +/- 60 mumol/min/100 mL glomerular filtration rate in the remnant kidney compared with 564 +/- 42 mumol/min/100 mL glomerular filtration rate in the normal kidney (P less than 0.01). Total renal ammoniagenesis per nephron increased to values found in chronic metabolic acidosis although serum (K+) and (HCO3-) were no different than in the normal dog. The oxidation of glutamine and lactate by remnant kidneys accounted for over 80% of Qo2, similar to that of normal kidneys. It is concluded that hypermetabolism per nephron occurs in the remnant kidney of the dog and that glutamine and lactate are the major energy substrates in remnant kidney. Furthermore, factors other than serum (K+) and (HCO3-) augment ammoniagenesis in this model. However, when these results are expressed per whole kidney or per gram of tissue, hypermetabolism does not occur in these remnant kidneys.(ABSTRACT TRUNCATED AT 250 WORDS)

Renal ammoniagenesis following glutamine loading in intact dogs during acute metabolic acid–base perturbations

1987 ◽  
Vol 72 (1) ◽  
pp. 61-69 ◽  
Author(s):  
Jorge Areas ◽  
Sevag Balian ◽  
Dianna Slemmer ◽  
Mario Belledonne ◽  
Harry G. Preuss
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Metabolic Acidosis ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Respiratory Acidosis ◽  
Glutamine Metabolism ◽  
Acid Base ◽  
Acute Metabolic Acidosis ◽  
Qualitative Changes

1. Adaptation of renal ammoniagenesis during acute metabolic acidosis in intact dogs may be nonexistent or, at least, markedly less than in chronic acidosis. This contrasts to adaptation in acute respiratory acidosis, where levels similar to those attained in chronic acidosis occur within hours. 2. Accordingly, the inability to discern marked changes in acute metabolic acidosis compared with acute respiratory acidosis has been attributed to decreased glomerular filtration rate and renal blood flow seen frequently in the former. 3. In our studies, we found early changes in ammoniagenesis and glutamine metabolism during acute metabolic acidosis, but not of the magnitude seen in chronic acidosis, even considering the changes in renal blood flow (RBF) and glomerular filtration rate (GFR). Exogenous glutamine loading allowed us to discover that the qualitative changes in glutamine metabolism during acute metabolic acidosis differed from control but fell short of those seen in chronic metabolic a acidosis. 4. We also examined glutamine metabolism when renal ammoniagenic adaptation was acutely inhibited in chronically acidotic dogs. Infusing NaHCO3 into chronically acidotic dogs decreased renal ammonia production significantly (247 μmol min−1 100 ml−1 GFR vs 148 μmol min−1 100 ml−1 GFR: P < 0.001) and glutamine extraction (111.8 μmol min−1 100 ml−1 GFR vs 90.9 μmol min−1 100 ml−1 GFR: P < 0.02). 5. The qualitative changes in renal glutamine metabolism in both studies suggest that alterations in deamination of glutamate formed from glutamine are responsible, at least in part, for adaptation to acute acid–base perturbations. 6. Compared with respiratory acidosis, adaptation to metabolic acidosis is progressive and prolonged.

Excretion of progastrin products in human urine

1999 ◽  
Vol 276 (4) ◽  
pp. G985-G992 ◽  
Author(s):  
C. Palnaes Hansen ◽  
J. P. Goetze ◽  
F. Stadil ◽  
J. F. Rehfeld
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Plasma Concentrations ◽  
Metabolic Clearance ◽  
Metabolic Clearance Rate ◽  
Renal Handling ◽  
Renal Metabolism ◽  
Tubular Transport ◽  
Excretion Rates

The renal handling of carboxyamidated gastrins, NH2-terminal progastrin fragments, and glycine-extended gastrins was examined in healthy volunteers. The respective urinary clearances after a meal amounted to 0.09 ± 0.02%, 0.17 ± 0.04% ( P< 0.05), and 0.04 ± 0.01% ( P< 0.01) of the glomerular filtration rate. During intravenous infusion of carboxyamidated gastrin-17, progastrin fragment-(1—35), and glycine-extended gastrin-17, the respective urinary clearances amounted to 0.08 ± 0.02, 0.46 ± 0.08, and 0.02 ± 0.01%, respectively, of the glomerular filtration rate. The metabolic clearance rate of the three peptides was 24.4 ± 1.3, 6.0 ± 0.4, and 8.6 ± 0.7 ml ⋅ kg−1⋅ min−1. A maximum rate for tubular transport or degradation of the peptides could not be determined, nor was a renal plasma threshold recorded. Plasma concentrations and urinary excretion rates correlated for gastrin-17 and progastrin fragment-(1—35) ( r = 0.94 and 0.97, P < 0.001), whereas the excretion of glycine-extended gastrin diminished with increasing plasma concentrations. We conclude that renal excretion of progastrin products is negligible compared with renal metabolism and that renal handling of the peptides depends on their molecular structure. Hence, the kidneys exhibited a higher excretion of NH2-terminal progastrin fragments than of carboxyamidated and especially glycine-extended gastrins.

Metabolic Acidosis Does Not Contribute to Chronic Renal Injury in the Rat

1995 ◽  
Vol 89 (6) ◽  
pp. 643-650 ◽  
Author(s):  
D. Throssell ◽  
J. Brown ◽  
K. P. G. Harris ◽  
J. Walls
Keyword(s):  
Renal Failure ◽  
Metabolic Acidosis ◽  
Chronic Renal Failure ◽  
Glomerular Filtration ◽  
Disease Progression ◽  
Renal Injury ◽  
Heart Weight ◽  
Normal Kidney ◽  
Renal Growth ◽  
Remnant Kidney

1. Metabolic acidosis invariably accompanies chronic renal failure, and short periods of metabolic acidosis cause renal growth and proteinuria in normal rats. Rates of ammoniagenesis are increased in chronic renal failure, and it has been suggested that this contributes to disease progression. This study assessed (i) whether prolonged acidosis causes chronic renal injury in the normal kidney and (ii) whether abrogation of acidosis slows disease progression in the remnant kidney. 2. Metabolic acidosis was induced in normal rats by dietary hydrochloric acid. Urinary excretion of total protein, lysozyme and albumin increased, peaking at week 8 but returning to baseline by week 14. At killing after 14 weeks, kidney weights, glomerular filtration rates and serum creatinine were the same in both groups, but kidney/body weight and kidney/heart weight ratios were greater in the acidotic group. All kidneys were normal by light microscopy. 3. Rats subjected to five-sixths nephrectomy were given sufficient dietary bicarbonate to abolish uraemic acidosis, and their outcome was compared with that of non-alkalinized remnants (controls). Proteinuria, glomerular filtration rates, blood pressure, histological injury and time to the development of terminal uraemia were no better in bicarbonate-supplemented animals than in controls. 4. These data demonstrate that metabolic acidosis neither causes nor exacerbates chronic renal injury. We conclude that the treatment of uraemic acidosis is unlikely to influence disease progression in patients with chronic renal failure.

Denosumab Improves Glomerular Filtration Rate in Osteoporotic Patients With Normal Kidney Function by Lowering Serum Phosphorus

2019 ◽  
Vol 34 (11) ◽  
pp. 2028-2035 ◽  
Author(s):  
Daichi Miyaoka ◽  
Masaaki Inaba ◽  
Yasuo Imanishi ◽  
Noriyuki Hayashi ◽  
Masaya Ohara ◽  
...  
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Kidney Function ◽  
Filtration Rate ◽  
Serum Phosphorus ◽  
Normal Kidney ◽  
Normal Kidney Function

scholarly journals Measurement of Glomerular Filtration Rate (GFR) in an Ectopic Pelvic Kidney by Dual Head Gamma Camera

2018 ◽  
Vol 20 (2) ◽  
pp. 114
Author(s):  
Hosne Ara Begum ◽  
Mahbub Ur Rahman ◽  
Samira Sharmin ◽  
Jesmin Ferdous ◽  
Jamiul Hossain
Keyword(s):  
Renal Function ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Correlation Coefficient ◽  
Gamma Camera ◽  
Filtration Rate ◽  
Pelvic Kidney ◽  
Normal Kidney ◽  
Ectopic Kidney ◽  
Gault Formula

<p><strong><em>Background</em></strong><em>:</em><strong> </strong>DTPA renogram is an accepted method to measure glomerular filtration rate (GFR) of the kidneys. The function of an ectopic kidney varies on the basis of its size, shape, position and rotation. This may lead to variation in tissue attenuation and error in computed GFR and differential renal function (DRF) of each kidney. The objectives of this study was to assess  the changes in the GFR measurement of an ectopic kidney in a dual head gamma camera using anterior and posterior imaging process and its influence on quantification of total GFR.</p><p><strong><em>Patients and Method:</em></strong><strong> </strong>A Total<strong> </strong>20 patients having one ectopic pelvic kidney and other normal positioning kidney were enrolled in the study. DTPA renogram images were acquired on a dual head gamma camera (Symbia T2) in anterior and posterior views simultaneously. Both anterior and posterior images data were used separately to compute the GFR. Three sets of total GFR of both kidneys were calculated separately. In set I, total GFR (ant) is equal to sum of both kidneys GFR in anterior imaging process, in set II total GFR (post) is equal to sum of both kidneys GFR in posterior imaging process and in set III total GFR (ectopic .ant + normal. post) is equal to sum of the GFR of normal kidney on posterior image and the GFR of ectopic kidney on anterior image. These three sets of total GFRs were compared with the patient’s eGFR measured by Cockcroft Gault formula.</p><p><strong><em>Result:</em></strong> Mean age of the patient was 36.9 ± 14.6 years (range 18-70 years). Mean total GFR (ant)   was 89.2±11.6 ml/min, total GFR (post) was 82.9±13.4 ml/min and total GFR (ectopic .ant + normal.post) was 102.5±15.9 ml/min. Mean eGFR is 101.93±24.9ml/min. When these three sets of DTPA assisted GFR compare with eGFR the Pearson’s correlation coefficient <em>r=</em> 0.45, 0.55 (P&lt;0.05) for GFR (ant) and GFR (post) respectively whereas, in case of GFR (ectopic .ant + normal.post) correlation coefficient <em>r=</em> 0.8 (P&lt;0.01).</p><p><strong><em>Conclusion:</em></strong> The GFR of ectopic kidney as calculated from the anterior data was significantly higher in comparison to the GFR calculated from the posterior data.</p><p>Bangladesh J. Nuclear Med. 20(2): 115-118, July 2017</p>

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