One- and five-year follow-ups on blood pressure and renal function in kidney donors.

It is considered safe to donate a kidney if internationally accepted medical criteria are fulfilled. However, some donors have encountered hypertension, proteinuria and impaired renal function after donation. The study was based on retrospective data on 908 donors, donating in the period 1997-2007. Preoperative and follow-up data were collected from patient files and the Norwegian Living Donor Registry. Follow-up data were available for 665 donors at 1 year after donation, and 256 donors at 5 years after donation. We calculated the estimated glomerular filtration rate (eGFR) using the four variable Modification of Diet in Renal Disease equation. At 1 and 5 years after donation, the prevalence of hypertension was 11.7% and 27.1% respectively compared to 2.6% before donation. Proteinuria was present in 3.3% and 1.6% at 1 and 5 years. Mean eGFR was 56.1 ± 10.8 ml/min/1.73 m² at 1 year and 61.0 ± 11.8 ml/min/1.73 m² at 5 years. Mean blood pressure was 122.5 ± 10.6/76.2 ± 7.5 mmHg at donation (n = 908), 124.3 ± 14.2/77.9 ± 8.2 mmHg at 1-year (n = 649) and 127.2 ± 15.4/78.8 ± 8.3 mmHg at 5-year follow-ups (n = 247). We found no evidence of further decline in renal function beyond the initial decrement following nephrectomy.

Undiagnosed diabetes in kidney transplant candidates: a case-finding strategy.

BACKGROUND AND OBJECTIVES: Guidelines recommend that candidates for kidney transplantation (KTx) who do not have diabetes perform a pretransplantation oral glucose tolerance test (OGTT) when fasting plasma glucose (FPG) is <110 mg/dl (<6.1 mmol/L); however, the OGTT is potentially costly and cumbersome. We studied the role of the OGTT for diagnosing diabetes and the accuracy of FPG and glycated hemoglobin (HbA(1c)) for predicting a diabetic OGTT before KTx. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: In this cross-sectional study, 889 first single-kidney transplant candidates without diabetes, mainly white, performed an OGTT during the transplantation workup. Results were studied using receiver operating characteristic analysis. RESULTS: Of 72 (8.1%) patients with undiagnosed diabetes, only 16 (22%) had a diabetic FPG (> or =126 mg/dl [> or =7.0 mmol/L]). In patients with a nondiabetic FPG, diabetes (2-hour plasma glucose [2h-PG] > or =200 mg/dl [> or =11.1 mmol/L]) was predicted by FPG but not by HbA(1c). Performing the OGTT in patients with FPG 92 to 125 mg/dl (5.1 to 6.9 mmol/L) identified 65 (90%) patients with diabetes (16 by FPG, 49 by 2h-PG) and required seven OGTTs per patient identified. Subjecting all patients with FPG <110 mg/dl (<6.1 mmol/L) to the OGTT identified 60 (83%) patients with diabetes (16 by FPG, 44 by 2h-PG) but required 14 OGTTs per patient. CONCLUSIONS: The OGTT was paramount in finding most cases of undiagnosed diabetes before KTx. FPG but not HbA(1c) predicted a diabetic OGTT. We suggest that white KTx candidates without diabetes perform a pretransplantation OGTT when FPG is 92 to 125 mg/dl (5.1 to 6.9 mmol/L).

Glucose tolerance before and after renal transplantation.

BACKGROUND: Renal insufficiency predisposes to insulin resistance, hyperparathyroidism and derangements in calcium phosphate and nitrogenous compound balance, leading to pre-transplant hyperglycaemia. These metabolic risk factors are not fully corrected after renal transplantation. The present study aimed to assess the role of pre-transplant glycaemia and the named metabolic risk factors in post-transplant hyperglycaemia [PHYG; impaired fasting glucose (IFG), impaired glucose tolerance (IGT) or diabetes mellitus (DM)]. METHODS: This is a retrospective cohort study involving 301 patients without pre-transplant DM. Measurements included a pre- and post-transplant oral glucose tolerance test (OGTT) as well as glomerular filtration rate (GFR), parathyroid hormone (PTH), phosphate, calcium and urea measured 10 weeks post-transplant. The risk of PHYG at 10 weeks post-transplant was analysed using multiple logistic regression. RESULTS: Ninety-three patients (31%) had PHYG (two IFG, 52 IGT, 39 DM). Variables associated with PHYG included pre-transplant 2-h glycaemia [OR 1.26, 95% CI (1.09, 1.46)] and post-transplant urea levels [OR 1.14, 95% CI (1.02, 1.27)]. Older age, non-Caucasian ethnicity, previous transplants, >or=3 HLA class 1 mismatches and high prednisolone doses were likewise associated with an increased PHYG risk (all P < 0.05). CONCLUSIONS: Pre-transplant glycaemia and high post-transplant levels of urea were associated with a greater risk of PHYG. This seemed to be independent of GFR, PTH, phosphate, calcium and traditional risk factors such as age and glucocorticoid load.

Role of prednisolone pharmacokinetics in postchallenge glycemia after renal transplantation.

Prednisolone may cause hyperglycemia after organ transplantation. Even at comparable weight-adjusted doses, prednisolone side effects vary considerably between individuals, suggesting between-patient pharmacokinetic differences. In renal transplant patients, assessment of glucocorticoid diabetogenicity is confounded by calcineurin inhibitors (CNIs). The present study aimed to investigate, in a CNI-free setting, the association between exposure to unbound prednisolone and glucose tolerance in stable nondiabetic long-term renal transplant patients. An oral glucose tolerance test and a 12-hour prednisolone pharmacokinetic study were performed in 108 nondiabetic CNI-naive subjects (41 women and 67 men) treated with prednisolone (median 0.15 mg kg d, interquartile range 0.14-0.18 mg kg d) and azathioprine. The area under the curve (AUC) of unbound prednisolone was analyzed in multiple linear regression analysis with 120-minute postchallenge glucose AUC as the dependent variable. A high AUC of unbound serum prednisolone was independently associated with a high glucose AUC (P = 0.030). A high glucose AUC was also associated with a high patient age and triglyceride level (both P < or = 0.001). No correlation was observed between the daily prednisolone dosage (mg/d or mg kg d) and glucose AUC. The association between exposure to unbound prednisolone and postchallenge glycemia is in line with current knowledge about mechanisms behind steroid-related side effects but has not previously been documented. The result may argue in favor of measuring unbound prednisolone in clinical settings. Increasing exposure to unbound prednisolone was independently associated with postchallenge glycemia. No such relationship was observed for prednisolone daily dose per se.