Rein et dysthyroïdies

Thyroid hormones influence renal development, kidney structure, renal hemodynamics, glomerular filtration rate, the function of many transport systems along the nephron, and sodium and water homeostasis. Effects of hypothyroidism and hyperthyroidism on kidney function are the result of direct renal effects, as well as systemic hemodynamic, metabolic, and cardiovascular effects. Most of the renal manifestations of thyroid disorders, which are clinically most significant with hypothyroidism, are reversible with treatment. Patients with hypothyroidism can have clinically important reductions in GFR, so screening for hypothyroidism should be considered in patients with unexplained elevations in serum creatinine. Patients with thyroid disorders are also at risk for immune-mediated glomerular diseases. Finally, patients with nephrotic syndrome, as well as acute and chronic kidney injury, have alterations in thyroid gland physiology that can impact thyroid function and the testing of thyroid function status. Dialysis patients have frequently hypothyroidism whose biological diagnosis must be careful.     

Lymphadenopathy and proteinuria.

Case A 79-year-old Vietnamese woman was hospitalized with a 2-monthhistory of progressive fatigue and dyspnoea. Her past historyincluded hypertension, hypercholesterolemia and cholecystectomy.Her physical examination revealed dyspnoea at rest, bilateralcrepitus, ascites, peripheral leg oedema, hypertension (150/100mmHg), ecchymosis, left subconjunctival haemorrhage jugulo-carotidianand axillary lymphadenopathies and barely palpable liver andspleen. Laboratory data are presented in Table 1; among them were serumcreatinine of 85 mmol/l, blood urea nitrogen 9.4 mmol/l, proteinuria(2.5–6 g/l) and     

Reappraisal of treatment-induced renal dysfunction in patients receiving antiangiogenic agents in phase I trials

Background Several phase I trials are currently evaluating new antiangiogenic compounds. While hypertension and proteinuria have been largely reported as a class side effect of these agents, data on renal function [i.e. the glomerular filtration rate (GFR)] in patients (pts) treated with new antiangiogenic compounds in phase I trials are much scarcer. Patients and methods Between November 2005 and March 2008, we identified 72 pts with solid tumors who had been included in four Phase I trials testing antiangiogenic or related compounds. Thirty-two pts had received a pan-HER/VEGFR inhibitor (A), 29 had received a vascular-disrupting agent (B) and 11 had received a pan-VEGFR inhibitor in combination with CPT11 (C). For each patient, we retrospectively analyzed the serum creatinine level (SCr), Cr clearance (CrCl) calculated by both the Cockcroft and Gault and aMDRD equations at baseline, during treatment and at the end of treatment. Acute renal failure (ARF) was defined as a decrease of >25% in CrCl, and severe renal failure (SRF) as a decrease of >50% in CrCl. Chronic renal failure (CRF) was defined according to the KDOQI-KDIGO classification. Renal dysfunction was defined as Cl <60 ml/min with a normal Cr level (<125 μmol/l). Results Each pt had received an average of 4 cycles of treatment (1 to 12). During treatment, the incidence of ARF ranged from 40.2% to 44.4% (A = 11/32, B = 19/29, C = 2/11). Seven to 9.7% of these cases were severe (A = 1/32, B = 6/29, C = 0/11). Moreover, 26.4 to 27.7% of the pts had exhibited persistent renal insufficiency at the end of the study (A = 5/32, B = 15/29, C = 0/11). From the start till the end of treatment, ARF had been documented in 20.8% to 22.2% of the pts. The average reduction in clearance was 9.8 to 11.6 ml/min/1.73 m2 between baseline and the end of treatment. Conclusion The incidence of renal toxicity in phase I pts treated with antiangiogenic compounds was much higher than expected. Simple screening of Cr levels appears to be insufficient and careful nephrologic monitoring at baseline and during treatment should be implemented in early clinical trials assessing the risk/benefit ratio of new antiangiogenic compounds.     

Abnormal blood pressure circadian rhythm: a target organ damage?

Blood pressure (BP) varies according to cycles characterized by a reduction during sleep and an increase on awakening. The nighttime decrease is absent or blunted in some patients (termed "non-dippers"). Cross-sectional and prospective data have shown that non-dippers have more target organ damage than have dippers in normotensive and hypertensive subjects. We reviewed the English language literature regarding this association. A non-fortuitous association seems to exist between non-dipper status and cardiovascular risk such as stroke and cardiac events. Among diabetic patients, this phenomenon has been described to occur more often in individuals with autonomic neuropathy and with different degrees of diabetic nephropathy. In normoalbuminuric normotensive type I diabetic patients without any degree of autonomic dysfunction, according to traditional cardiovascular tests, diastolic BP (dBP) night/day ratio is associated with an increased glomerular filtration rate and an increased extracellular volume. The disruption of the circadian rhythm of sympathovagal activity in non-dipper patients was associated with higher levels in systolic BP (sBP) and dBP and with a reduced decline in sBP and dBP levels during the night. Therefore, the prognostic implications of the non-dipper status may be important since the overall 24-h blood pressure load is elevated in these individuals. These data suggest that patients in whom blood pressure decreases during the night incur less damage to their brain, kidneys, heart, and blood vessels than people with elevated nocturnal BP.