Chemosensory function and food preferences among haemodialysis patients.

INTRODUCTION: Malnutrition and disturbed sense of smell and taste frequently occur in patients treated with chronic haemodialysis. The common denominator between chemosensation and nutrition may be food preferences. Our aim was to investigate smell and taste function as well as food preferences among haemodialysis patients and compare the results with those of age-matched controls. METHODS: An observational case-control study was conducted on 29 patients on chronic haemodialysis and 39 age-matched healthy controls. Chemosensory function was evaluated using validated gustatory and olfactory tests. Food preferences were recorded using a questionnaire of 63 items including a five-point Likert scale of familiarity, liking and frequency. RESULTS: Chemosensory function was significantly poorer among patients than among controls. Patients had significantly lower familiarity and frequency of consumptions of all food categories than controls and they also had significantly lower liking of vegetables, fruits and starches. CONCLUSIONS: Implementation of the provided knowledge about haemodialysis patients' smell and taste function including their food preferences are suggested, such as enhancement of odorant intensity, use of taste amplification, cooking habits and exposure to more varied food items. Assessments of food preferences and chemosensory function prior to determination of individual dietary schedules are therefore recommended. FUNDING: The authors did not receive any financial support for the research or drafting of this article. The authors declare that they have no financial interests to report. TRIAL REGISTRATION: Danish Ethical Committee project number: M-2018-188-18.

Urothelial Carcinoma in an Allograft kidney.

Patients who have been kidney transplanted have an increased risk of developing cancer. This case report presents a rarely described case in which a patient, who had received a kidney transplant from a deceased donor, was diagnosed with disseminated urothelial carcinoma originating from the allograft. After the removal of the allograft and the immunosuppressive treatment, there was regression in the cancer. Unfortunately, it was not a complete regression of the urothelial cancer and the patient died. This case indicates that there is a risk of getting cancer from the transplanted kidney from a deceased donor, but also that the immunosuppressive treatment can contribute to the development of this cancer.

Effect of tolvaptan on renal handling of water and sodium, GFR and central hemodynamics in autosomal dominant polycystic kidney disease during inhibition of the nitric oxide system: a randomized, placebo-controlled, double blind, crossover study.

BACKGROUND: Tolvaptan slows progression of autosomal dominant polycystic kidney disease (ADPKD) by antagonizing the vasopressin-cAMP axis. Nitric oxide (NO) stimulates natriuresis and diuresis, but its role is unknown during tolvaptan treatment in ADPKD. METHODS: Eighteen patients with ADPKD received tolvaptan 60 mg or placebo in a randomized, placebo-controlled, double blind, crossover study. L-NMMA (L-NG-monomethyl-arginine) was given as a bolus followed by continuous infusion during 60 min. We measured: GFR, urine output (UO), free water clearance (CH2O), fractional excretion of sodium (FENa), urinary excretion of aquaporin-2 channels (u-AQP2) and epithelial sodium channels (u-ENaCγ), plasma concentrations of vasopressin (p-AVP), renin (PRC), angiotensinII (p-AngII), aldosterone (p-Aldo), and central blood pressure (cBP). RESULTS: During tolvaptan with NO-inhibition, a more pronounced decrease was measured in UO, CH2O (61% vs 43%) and FENa (46% vs 41%) after placebo than after tolvaptan; GFR and u-AQP2 decreased to the same extent; p-AVP increased three fold, whereas u-ENaCγ, PRC, p-AngII, and p-Aldo remained unchanged. After NO-inhibition, GFR increased after placebo and remained unchanged after tolvaptan (5% vs -6%). Central diastolic BP (CDBP) increased to a higher level after placebo than tolvaptan. Body weight fell during tolvaptan treatment. CONCLUSIONS: During NO inhibition, tolvaptan antagonized both the antidiuretic and the antinatriuretic effect of L-NMMA, partly via an AVP-dependent mechanism. U-AQP2 was not changed by tolvaptan, presumeably due to a counteracting effect of elevated p-AVP. The reduced GFR during tolvaptan most likely is caused by the reduction in extracellular fluid volume and blood pressure. TRIAL REGISTRATION: Clinical Trial no: NCT02527863 . Registered 18 February 2015.

Effect of sodium nitrite on renal function and sodium and water excretion and brachial and central blood pressure in healthy subjects: a dose-response study.

Sodium nitrite (NaNO2) is converted to nitric oxide (NO) in vivo and has vasodilatory and natriuretic effects. Our aim was to examine the effects of NaNO2 on hemodynamics, sodium excretion, and glomerular filtration rate (GFR). In a single-blinded, placebo-controlled, crossover study, we infused placebo (0.9% NaCl) or 0.58, 1.74, or 3.48 µmol NaNO2·kg-1·h-1 for 2 h in 12 healthy subjects, after 4 days of a standard diet. Subjects were supine and water loaded. We measured brachial and central blood pressure (BP), plasma concentrations of renin, angiotensin II, aldosterone, arginine vasopressin (P-AVP), and plasma nitrite (P-[Formula: see text]), GFR by Cr-EDTA clearance, fractional excretion of sodium (FENa) free water clearance (CH2O), and urinary excretion rate of guanosine 3',5'-cyclic monophosphate (U-cGMP). The highest dose reduced brachial systolic BP (5.6 mmHg, P = 0.003), central systolic BP (5.6 mmHg, P = 0.035), and CH2O (maximum change from 3.79 to 1.27 ml/min, P = 0.031) and increased P-[Formula: see text] (from 0.065 to 0.766 µmol/l, P < 0.001), while reducing U-cGMP (from 444 to 247 pmol/min, P = 0.004). GFR, FENa, P-AVP, and the components in the renin-angiotensin-aldosterone system did not change significantly. In conclusion, intravenous NaNO2 induced a dose-dependent reduction of brachial and central BP. The hemodynamic effect was not mediated by the renin-angiotensin-aldosterone system. NaNO2 infusion resulted in a vasopressin-independent decrease in CH2O and urine output but no change in urinary sodium excretion or GFR. The lack of increase in cGMP accompanying the increase in [Formula: see text] suggests a direct effect of nitrite or nitrate on the renal tubules and vascular bed with little or no systemic conversion to NO.

Effects of atorvastatin on systemic and renal nitric oxide in healthy man.

Statin treatment improves endothelial function but the effects of statins on renal nitric oxide have not been clarified. In this crossover study, 26 healthy subjects received atorvastatin 80 mg per day or placebo for 5 days. After 5 days of treatment, L-N(G)-monomethyl arginine caused a similar increase in blood pressure and decrease in urine output and glomerular filtration rate. The decrease in fractional excretion of sodium to L-N(G)-monomethyl arginine was more pronounced after atorvastatin treatment. Atorvastatin did not change the response to several vasoactive hormones. The results indicate that atorvastatin increase renal nitric oxide, which may explain a part of the pleiotropic effects of statins.

Effect of nitric oxide inhibition on blood pressure and renal sodium handling: a dose-response study in healthy man.

Nitric oxide (NO) is a ubiquitous vasodilator and an important regulator of renal sodium excretion. To further investigate the role of NO in renal sodium handling, we studied the effects of the NO synthase inhibitor, NG-monomethyl-L-arginine (L-NMMA), in a crossover dose-response study. During NO inhibition mean arterial pressure increased dose-dependently and reached a plateau after 20 minutes of infusion. On the contrary, the fractional excretion of sodium was reduced equally in all three L-NMMA doses. This indicates that sodium excretion is highly sensitive to even small changes in renal NO bioavailability in healthy human.