Biomedical subjects

H N Ibrahim

Publications and source records attributed to H N Ibrahim.

8 recordsLinked to original sources

PubMed2006

Predictors of chronic kidney disease in long-term survivors of lung and heart-lung transplantation.

Renal insufficiency is common after non-renal organ transplants. The predictors of long-term renal outcomes are not well established. A total of 219 lung and heart-lung transplant recipients surviving more than 6 months after transplantation were studied to determine predictors of time to doubling of serum creatinine and end-stage kidney disease (ESKD) with death as a competing risk. Median follow-up was 79 months (range 9-222 months). Baseline estimated glomerular filtration rate (GFR) was 96.3+/-34.5 mL/min/1.73 m2. One hundred twenty-two recipients (55%) doubled their serum creatinine, 16 (7.3%) progressed to ESKD and 143 (65%) died. The majority of recipients who survived >6 years had a GFR<60 mL/min at both 1 and 7 years. Most of the loss of renal function occurred in the first year post-transplant. Older age at transplant, lower GFR at 1 month and cyclosporine use in the first 6 months predicted shorter time to doubling of serum creatinine when death was handled as a competing risk. Based on this prevalence data and using GFR decay and death as study endpoints, we offer sample size estimates for a prospective, interventional trial that is aimed at slowing or preventing the progression of kidney disease.

Creatinine↗

PubMed2006

The performance of three serum creatinine-based formulas in estimating GFR in former kidney donors.

Studies addressing long-term consequences of living with one kidney have used serum creatinine-based formulas that have not been validated in former kidney donors. Therefore, we evaluated the performance of Cockcroft-Gault (CG), Modification of Diet in Renal Disease (MDRD) and Mayo Clinic formulas in predicting iohexol glomerular filtration rate (iGFR) after donation in 112 randomly selected former kidney donors. Mean time from donation was 12.2 +/- 8.5 years. Serum creatinine was 1.1 +/- 0.2 mg/dL and iohexol GFR was 72 +/- 12 mL/min/1.73 m(2). The majority, 83.9%, of donors had a GFR >60 mL/min. CG formula overestimated GFR by 3.35 +/- 13.6 mL/min and was within 10% of iohexol GFR in only 43.7% of cases. MDRD formula underestimated iohexol GFR by 6.45 +/- 9.5 mL/min and was within 10% of actual GFR in half of the cases. In contrast, the Mayo Clinic equation was the most biased at 14.71 +/- 12.3 mL/min and was within 10% of measured GFR in only a fifth of the cases. Only MDRD and CG formulas provide estimates of GFR in former kidney donors that are within a clinically acceptable range of actual GFR. In conclusion, the majority of former kidney donors have excellent kidney function and the MDRD formula should be the recommended GFR estimating model in this population.

Biomarkers↗

PubMed2001

Aldosterone in progressive renal disease.

Blockade of the renin-angiotensin-aldosterone system has proven effective in retarding progression of renal disease in the remnant kidney model, as well as other experimental diseases, and, most importantly, in a range of progressive human renal diseases. Attention has focused on the role of angiotensin II (Ang II) in propagating progression both by its hemodynamic and nonhemodynamic actions. Recent evidence, predominately in the remnant kidney model, indicates that the drugs used to block this hormone system, angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers, also lower aldosterone levels. Thus, aldosterone, as well as angiotensin II, appears to be instrumental in sustaining the hypertension and fibroproliferative destruction of the residual kidney.

Aldosterone↗

PubMed2001

Aldosterone in renal disease.

Blockade of the renin-angiotensin-aldosterone system has proved effective in retarding the progression of renal disease in the remnant kidney model, as well as other experimental diseases, and most importantly, in a range of progressive human renal diseases. Attention has focused on the role of angiotensin II in propagating progression both by its hemodynamic and non-hemodynamic actions. Recent evidence, predominantly in the remnant kidney model, indicates that the drugs used to block this hormone system, angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers, also lower aldosterone levels. Aldosterone as well as angiotensin II thus appears to be instrumental in sustaining the hypertension and fibroproliferative destruction of the residual kidney.

Aldosterone↗

PubMed1998

The renin-aldosterone axis in two models of reduced renal mass in the rat.

The renin-angiotensin-aldosterone system participates in chronic progressive renal disease. The studies presented here assessed the importance of aldosterone in two different methods of reduced kidney mass in the rat, i.e., the infarction model (INF; uninephrectomy plus infarction of approximately two-thirds of the other kidney) and surgical excision or polectomy (POL; uninephrectomy plus surgical excision of both poles of the other kidney). Equivalent degrees of reduction in renal mass were confirmed by the similarity of serum creatinines 3 d after the ablative procedure. Measurements were made thereafter at 2 and 4 wk postablation. Systolic arterial pressure was greater with INF at both 2 and 4 wk. Proteinuria was also greater in the INF group at both time periods. The percentage of glomeruli with sclerosis measured at 4 wk tended to be greater in the INF group; however, this difference was not of statistical significance. At 2 wk, plasma renin activity and plasma aldosterone levels were lower in the POL group. The renin concentration in the scar region of the kidneys in the INF group was higher than in the kidney of the POL group. In conjunction with the lower plasma aldosterone, rats in the POL group had higher plasma potassium concentrations at 2 wk. In summary, higher aldosterone and plasma renin levels distinguish the INF model from the POL and likely contribute to the greater proteinuria and hypertension in the INF model.

Animals↗

PubMed1997

Diabetic nephropathy.

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Diabetes Mellitus, Type 1↗

PubMed1997

Role of the renin-angiotensin-aldosterone system in the progression of renal disease: a critical review.

Interruption of the renin-angiotensin-aldosterone system (RAAS) by converting enzyme inhibition or angiotensin II (ANG II) receptor antagonism dramatically reduces injury in the remnant kidney model. Furthermore, converting enzyme inhibition reduces proteinuria and slows the decline in renal function in clinical disease. Hemodynamic actions of ANG II in the kidney in conjunction with a more poorly defined effect of the RAAS on systemic hypertension have been posited as the major mechanisms for maintenance of elevated glomerular pressure. Reductions in glomerular pressure have been attributed, at least in part, to removal of intrarenal effects of ANG II. Growth and fibrotic actions of ANG II may also contribute to progressive renal injury and relief from them reduce injury. The participation of circulating aldosterone in the remnant kidney model has been recently raised. Hyperaldosteronism and adrenal hypertrophy attend the hypertension, proteinuria, and glomerulosclerosis of this model. Although the hemodynamic actions of aldosterone probably account for some of the adverse effects it has in this model, other direct cellular actions may participate in its renal, as well as cardiac and fibrotic consequences. Thus, the RAAS, working through both ANG II and aldosterone, contributes to chronic progressive renal injury.

Angiotensin II↗

PubMed1997

Aldosterone is a major factor in the progression of renal disease.

There is compelling evidence supporting the renin-angiotensin-aldosterone system contribution in experimental and human renal disease. Interruption of this system by converting enzyme inhibition or angiotensin II receptor antagonism reduces injury. Angiotensin II contributes to the progression of renal disease through its direct vascular effects and proliferative properties. The mediators of angiotensin II induced renal injury are many and include TGF-beta, PDGF, bFGF, and endothelin. Though the mechanisms involved in its contribution to progressive renal disease are not well delineated, aldosterone seems to be an overlooked contributor to the progression of kidney disease and its effects may also depend on both its hemodynamic and more direct cellular actions.

Aldosterone↗