Streptozotocin-induced renal hemodynamic changes in isogenic Lewis rats: a kidney transplant study

1993 ◽  
Vol 264 (1) ◽  
pp. F100-F105 ◽  
Author(s):  
P. Churchill ◽  
M. Churchill ◽  
A. Bidani ◽  
J. Dunbar
Keyword(s):  
Diabetes Mellitus ◽  
Experimental Model ◽  
Kidney Transplant ◽  
Left Kidney ◽  
Hemodynamic Changes ◽  
Lewis Rats ◽  
Diabetic State ◽  
Renal Hemodynamic ◽  
Renal Clearances ◽  
Per Se

Streptozotocin (STZ)-induced diabetes mellitus is associated with decreased renal clearances of inulin and p-aminohippurate (PAH). The present experiments were designed to determine whether STZ-induced renal hemodynamic changes are due to the drug per se, rather than to the diabetic state that it induces. Isogenic Lewis rats with native right and transplanted left kidneys were studied. In one group, kidney donors received 50 mg STZ/kg body wt on day 1 and transplantation was performed on day 4 (untreated recipients). On day 29, the inulin and PAH clearances of these nondiabetic recipients were, respectively, 0.94 +/- 0.04 and 2.58 +/- 0.11 ml.min-1 x g-1 for the transplanted left kidney (previously exposed to STZ) and 0.95 +/- 0.07 and 2.54 +/- 0.14 ml.min-1 x g-1 for the native right kidney (never exposed to STZ). In another group, recipients received STZ on day 1 and transplantation was performed on day 4 (untreated donors). On day 29, the inulin and PAH clearances of these diabetic recipients were, respectively, 0.62 +/- 0.04 and 1.46 +/- 0.11 ml.min-1 x g-1 for the transplanted left kidney (never exposed to STZ) and 0.61 +/- 0.05 and 1.42 +/- 0.08 ml.min-1 x g-1 for the native right kidney (previously exposed to STZ). We conclude that the diabetic state, rather than STZ, is responsible for the decreased renal clearances of inulin and PAH in this experimental model.

Renal hemodynamic changes and renal functional reserve in children with type I diabetes mellitus

2007 ◽  
Vol 22 (11) ◽  
pp. 1903-1909 ◽  
Author(s):  
Ann Raes ◽  
Raymond Donckerwolcke ◽  
Margarita Craen ◽  
Maraina Che Hussein ◽  
Johan Vande Walle
Keyword(s):  
Diabetes Mellitus ◽  
Type I Diabetes ◽  
Type I Diabetes Mellitus ◽  
Type I ◽  
Hemodynamic Changes ◽  
Functional Reserve ◽  
Renal Functional Reserve ◽  
Renal Hemodynamic

Harnsäure, Nierenerkrankungen und Nephrolithiasis

2016 ◽  
Vol 73 (3) ◽  
pp. 159-165 ◽  
Author(s):  
Min Jeong Kim ◽  
Helmut Hopfer ◽  
Michael Mayr
Keyword(s):  
Diabetes Mellitus ◽  
Diabetes Mellitus Typ 2 ◽  
Therapeutische Konsequenzen ◽  
Per Se

Zusammenfassung. Verschiedene Nierenerkrankungen können mit erhöhten Harnsäurewerten einhergehen, wobei die pathophysiologischen Vorgänge sich stark unterscheiden. Dies ist nicht nur von akademischer Bedeutung, sondern hat auch wichtige therapeutische Konsequenzen. Während ein massiver und plötzlicher Harnsäure-Anfall im Rahmen eines Tumor-Lyse-Syndroms zum akuten Nierenversagen führen kann, liegen der umstrittenen chronischen Urat-Nephropathie dauerhaft erhöhte Harnsäurewerte zugrunde. Möglicherweise ist hier das entscheidende Agens aber gar nicht die Hyperurikämie per se, sondern Blei, zumindest gibt es diese Assoziation. Bei der Nephrolithiasis mit Harnsäuresteinen ist der entscheidende Faktor nicht wie zu vermuten wäre eine Hyperurikämie oder Hyperurikosurie, sondern eine Azidifikationsstörung auf renaler Ebene mit persistierend tiefem Urin-pH. Es gibt starke Hinweise, dass die beiden metabolischen Erkrankungen Adipositas und der Diabetes mellitus Typ 2 mit Insulinresistenz wichtige pathophysiologische Faktoren in der Entstehung dieser Azidifikationsstörung sind. Patienten mit Harnsäuresteinen sollten deshalb immer auf das Vorliegen dieser metabolischen Faktoren abgeklärt und dementsprechend behandelt werden.

Urinary metabolites of thromboxane and prostacyclin in diabetes mellitus

1988 ◽  
Vol 118 (2) ◽  
pp. 301-305 ◽  
Author(s):  
K. Gréen ◽  
O. Vesterqvist ◽  
V. Grill
Keyword(s):  
Diabetes Mellitus ◽  
Mass Spectrometry ◽  
Gas Chromatography ◽  
Insulin Treatment ◽  
Artificial Pancreas ◽  
Urinary Metabolites ◽  
Gas Chromatography Mass Spectrometry ◽  
Diabetic State ◽  
In Vivo Synthesis

Abstract. The in vivo synthesis of thromboxane A2 and prostacyclin was estimated in 23 diabetics through measurements of the major urinary metabolites 2,3-dinor-thromboxane B2 and 2,3-dinor-6-keto-PGF1α utilizing gas chromatography-mass spectrometry. Mean excretion was similar to that in non-diabetic subjects. The possible influence of hyperglycemia on the excretion of 2,3-dinor-thromboxane B2 and 2,3-dinor-6-keto-PGF1α was evaluated in three ways: by measuring excretion before and during an acute 9-h normalization of hyperglycemia through an artificial pancreas (Biostator) as well as by comparing excretion before and 7–12 days or 40–180 days after the initiation of insulin treatment. Despite significant reducing effects on hyperglycemia or on levels of hemoglobin A1c, no effects on the excretion of the thromboxane and prostacyclin metabolites could be found. Abnormal formation of thromboxane or prostacyclin is not a generalized feature of the diabetic state.

scholarly journals Current Pharmacological Intervention and Medical Management for Diabetic Kidney Transplant Recipients

Pharmaceutics ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 413
Author(s):  
Theerawut Klangjareonchai ◽  
Natsuki Eguchi ◽  
Ekamol Tantisattamo ◽  
Antoney J. Ferrey ◽  
Uttam Reddy ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Kidney Transplantation ◽  
Kidney Transplant ◽  
Pharmacological Intervention ◽  
Diabetic Patients ◽  
Transplant Recipients ◽  
Kidney Transplant Recipients ◽  
Kidney Allograft ◽  
Post Transplant ◽  
Glucose Management

Hyperglycemia after kidney transplantation is common in both diabetic and non-diabetic patients. Both pretransplant and post-transplant diabetes mellitus are associated with increased kidney allograft failure and mortality. Glucose management may be challenging for kidney transplant recipients. The pathophysiology and pattern of hyperglycemia in patients following kidney transplantation is different from those with type 2 diabetes mellitus. In patients with pre-existing and post-transplant diabetes mellitus, there is limited data on the management of hyperglycemia after kidney transplantation. The following article discusses the nomenclature and diagnosis of pre- and post-transplant diabetes mellitus, the impact of transplant-related hyperglycemia on patient and kidney allograft outcomes, risk factors and potential pathogenic mechanisms of hyperglycemia after kidney transplantation, glucose management before and after transplantation, and modalities for prevention of post-transplant diabetes mellitus.

scholarly journals Concentration of tacrolimus and major metabolites in kidney transplant recipients as a function of diabetes mellitus and cytochrome P450 3A gene polymorphism

Xenobiotica ◽  
2013 ◽  
Vol 43 (7) ◽  
pp. 641-649 ◽  
Author(s):  
Shripad D. Chitnis ◽  
Ken Ogasawara ◽  
Björn Schniedewind ◽  
Reginald Y. Gohh ◽  
Uwe Christians ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Cytochrome P450 ◽  
Gene Polymorphism ◽  
Kidney Transplant ◽  
Transplant Recipients ◽  
Cytochrome P450 3A ◽  
Kidney Transplant Recipients

Functional evidence for renorenal reflexes in the rat

1980 ◽  
Vol 239 (3) ◽  
pp. F265-F270 ◽  
Author(s):  
R. E. Colindres ◽  
W. S. Spielman ◽  
N. G. Moss ◽  
W. W. Harrington ◽  
C. W. Gottschalk
Keyword(s):  
Filtration Rate ◽  
Renal Denervation ◽  
Left Kidney ◽  
Mean Value ◽  
Urinary Volume ◽  
Hemodynamic Changes ◽  
Nerve Activity ◽  
Functional Changes ◽  
Simultaneous Decrease ◽  
The Right

Acute left renal denervation in anesthetized volume-expanded rats produced an ipsilateral diuresis and natriuresis in 19 animals. A simultaneous decrease of glomerular filtration rate, p-aminohippurate clearance, urinary volume (P < 0.002), and percentage of filtered sodium excreted (4.0 +/- 0.6 (SE) vs. 1.9 +/- 0.4%, P < 0.003) occurred in the right innervated kidney in 10 rats. Prior denervation of the right kidney in the other nine rats prevented the renal hemodynamic changes and the fall of urinary volume and of sodium excretion (3.9 +/- 0.6 vs. 4.3 +/- 0.5%) by the right kidney after left renal denervation. Nerve traffic to the right kidney was measured in six other animals after left renal denervation and was found to increase to a mean value 33.8 +/- 6.3% above control levels (P < 0.007) 0-30 min after denervation, with a further significant increase to 66.2 +/- 16.1% above control levels (P < 0.025) 30-60 min after denervation. These results indicate that the functional changes in the right kidney after contralateral renal denervation in volume-expanded rats are caused by a reflex increase in nerve traffic to the right kidney, possibly as a consequence of an interruption of afferent nerve activity originating in the left kidney.

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