Reflex sympathetic dystrophy syndrome of the lower limbs in a renal transplant patient treated with tacrolimus.

BACKGROUND: Recently, a previously unrecognized posttransplant syndrome known as reflex sympathetic dystrophy syndrome of the lower limbs has emerged in patients receiving cyclosporine as immunosuppression. We describe herein this complication observed in a patient treated with tacrolimus after kidney transplantation. METHODS: A 49-year-old man received a kidney transplant from a cadaver donor and was treated with tacrolimus. Three months later, the patient complained of severe pain in the lower limbs that affected both knees and ankles. Bone scintigraphy and magnetic resonance were consistent with reflex sympathetic dystrophy syndrome. RESULTS: Laboratory tests that included creatinine, glomerular filtration rate, calcium, phosphate, urate, alkaline phosphatase, and parathormone were normal or near normal. Tacrolimus levels were around 13 microg/ml. Clinical improvement appeared slowly and spontaneously during the following 3 months, without appreciable changes in the tacrolimus level. CONCLUSIONS: In kidney transplant patients, tacrolimus could be a risk factor for the development of a reflex sympathetic dystrophy syndrome.

Hypertension and nephrotoxicity in the rate of decline in kidney function in diabetic nephropathy.

Serum creatinine levels were determined prospectively every 2 to 3 months in 40 patients with diabetic nephropathy for a global observation period of 864 months. The monthly creatinine increasing rate was significantly lower in normotensive periods, mean arterial pressure (MAP) less than 115 mmHg, when compared with hypertensive periods, MAP greater than 125 mmHg. No significant difference was shown in periods with borderline hypertension (MAP between 115-124 mmHg). The mean creatinine increases were of 0.036 mg/dl/month, 0.3 mg/dl/month and 0.046 mg/dl/month respectively. Normotension was associated with a slowing down of the rate of decline in renal function in this group of moderate kidney failure with an initial mean serum creatinine of 2.26 mg/dl. The exposure of patients to nephrotoxics (aminoglycosides, and possibly anesthesia) significantly accelerated the decline in renal function: 0.39 mg/dl/month and 0.17 mg/dl/month respectively according to the concomitance or not of toxics and hypertension. The reported protective effect of diabetes against aminoglycosides nephrotoxicity in experimental conditions was not reflected in our clinical results. On the contrary, we suggest a possible enhanced sensibility of the diabetic patient with diabetic nephropathy to aminoglycosides leading to an acceleration of the progression of renal failure.