[Are thiazide diuretics ineffective with a glomerular filtration rate lower than 50 ml/min?] / Thiaziddiuretika unwirksam bei einer glomerulären Filtrationsrate kleiner als 50 ml/min?

Many treatment guidelines do not recommend the use of thiazide diuretics or thiazide-like diuretics in patients with impaired kidney function. The rationale is a presumed lack of efficacy of these diuretics in cases of a reduced glomerular filtration rate (GFR); however, this paradigm could not be verified in recent studies. Thiazide diuretics and thiazide-like diuretics are also effective in patients with substantially reduced GFR, which pertains to natriuresis, correction of volume overload and lowering of blood pressure; however, in patients with chronic kidney disease loop diuretics can control volume overload more rapidly. Particularly effective is the combination of loop diuretics with thiazide diuretics or thiazide-like diuretics in patients with markedly limited GFR. Therefore, thiazide diuretics and thiazide-like diuretics should also be prescribed even for patients with higher grade impairments of kidney function (chronic kidney disease in stages 3-5), except for anuric patients where they are ineffective.

Hypertension after kidney transplantation

Modern immunosuppressive drugs have greatly improved short time kidney graft survival, however, are associated with a high prevalence of hypertension in kidney transplant recipients, approaching 90 per cent. The use of calcineurin inhibitors is a major cause of hypertension after kidney transplantation, other significant causes are impaired graft function - due to chronic allograft nephropathy or other types of graft disease including recurrence of primary disease - humoral or neurogenic pressor signals arising from the graft or the diseased kidneys, stenotic lesions of arteries supplying the graft, possibly also a genetic predisposition to hypertension of the graft donor. Hypertension in renal allograft recipients is of major prognostic relevance for graft survival but also for cardiovascular disease in the recipients. Even modest elevations of blood pressure are associated with premature graft loss. Recipient systolic blood pressure is one of the best predictors. Hypertension amplifies vascular injury in the graft and accelerates the deleterious effects of other non-immunologic, e.g. hyperlipidemia, and immunologic factors e.g. chronic rejection, promoting graft loss. Aggressive treatment of hypertension in renal transplant patients mandatory, blood pressure should be lowered to < 130/85 mmHg or even lower. Apart from general measures, such as sodium restriction, weight loss programs, physical exercise or angioplasty in the case of kidney graft artery stenos antihypertensive treatment is required in most cases. Calcium antagonists, angiotensin converting enzyme inhibitors and diuretics are drugs of first choice. Studies are required assess the effects of calcineurin inhibitor withdrawal on post-transplant hypertension and long-term patient and graft survival after kidney transplantation.