The risk of PTDM increases continuously with time post-transplant. There has been an increase in the incidence of PTDM in patients transplanted recently, and that increase can be explained only partially by changes in the recipients' characteristics. We postulate that this increase may be due to the introduction of better absorbed CsA formulations that result in higher blood levels and higher cumulative exposure to this diabetogenic drug.
s: PTDM is associated with an unfavorable cardiovascular risk profile that precedes the development of hyperglycemia. PTDM is an independent predictor of reduced survival in renal allograft recipients.
The most common cause of thrombotic microangiopathy (TMA) in renal allografts is thought to be calcineurin inhibitor toxicity. Antibody-mediated rejection (AMR) can also cause TMA, but its true impact on de novo TMA is unknown. In a retrospective review of renal allograft biopsies from January 2003 to December 2008 at our institution, we determined the prevalence of TMA in patients with C4d positive (n = 243) and C4d negative (n = 715) biopsies. Over 90% of patients received cyclosporine in both groups. De novo TMA was seen in 59 (6.1%) patients; most of them (55%) with C4d positive biopsy. Among patients with C4d positive biopsies, 13.6% had TMA, as compared to only 3.6% patients with C4d negative biopsies (p < 0.0001). Incidence of graft loss between C4d positive and C4d negative TMA groups was not significantly different, but 70% of patients with C4d positive TMA who received plasmapheresis had slightly lower graft loss rate. In biopsies with AMR-associated TMA, glomerulitis and peritubular capillaritis were significantly more prominent. AMR is the most common cause of TMA in renal allografts in our patient population. It is important to recognize AMR-related TMA because plasmapheresis treatment may be beneficial.
Background
There have been few prospective controlled studies of kidney donors.
Understanding the pathophysiological effects of kidney donation is important for judging donor safety and for improving our understanding of the consequences of reduced kidney function in chronic kidney disease.
Study Design
Prospective, controlled, observational cohort study.
Setting & Participants
Three-year follow-up of kidney donors and paired controls suitable for donation at their donor’s center.
Predictor
Kidney donation.
Outcomes
Medical history, vital signs, glomerular filtration rate and other measurements at 6, 12, 24 and 36 months after donation.
Results
At 36 months, 182 of 203 (89.7%) original donors and 173 of 201 (86.1%) original controls continue to participate in follow-up visits. The linear slope of the glomerular filtration rate measured by plasma iohexol clearance declined 0.36±7.55 mL/min per year in 194 controls, but increased 1.47±5.02 mL/min per year in 198 donors (P = 0.005) between 6 and 36 months. Blood pressure was not different between donors and controls at any visit, and at 36 months all 24-hour ambulatory blood pressure parameters were similar in 126 controls and 135 donors (mean systolic: 120.0±11.2 [SD] v. 120.7±9.7 mmHg [P=0.6]; mean diastolic: 73.4±7.0 v. 74.5±6.5 mmHg [P=0.2]). Mean arterial pressure nocturnal dipping was manifest in 11.2%±6.6% of controls and 11.3%±6.1% donors (P=0.9). Urinary protein-creatinine and albumin-creatinine ratios were not increased in donors compared to controls. From 6 to 36 months post-donation, serum parathyroid hormone, uric acid, homocysteine and potassium levels were higher, whereas hemoglobin was lower in donors compared to controls.
Limitations
Possible bias resulting from an inability to select controls screened to be as healthy as donors, short follow-up duration, and drop-outs.
Conclusions
Kidney donors manifest several of the findings of mild chronic kidney disease. However, at 36 months after donation, kidney function continues to improve in donors while controls have expected age-related declines in function.
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