Usefulness of the 2-year iodine-123 metaiodobenzylguanidine-based risk model for post-discharge risk stratification of patients with acute decompensated heart failure.

PURPOSE: A four-parameter risk model that included cardiac iodine-123 metaiodobenzylguanidine (MIBG) imaging and readily available clinical parameters was recently developed for prediction of 2-year cardiac mortality risk in patients with chronic heart failure. We sought to validate the ability of this risk model to predict post-discharge clinical outcomes in patients with acute decompensated heart failure (ADHF) and to compare its prognostic value with that of the Acute Decompensated Heart Failure National Registry (ADHERE) and Get With The Guidelines-Heart Failure (GWTG-HF) risk scores. METHODS: We studied 407 consecutive patients who were admitted for ADHF and survived to discharge, with definitive 2-year outcomes (death or survival). Cardiac MIBG imaging was performed just before discharge. The 2-year cardiac mortality risk was calculated using four parameters, namely age, left ventricular ejection fraction, New York Heart Association functional class, and cardiac MIBG heart-to-mediastinum ratio on delayed images. Patients were stratified into three groups based on the 2-year cardiac mortality risk: low- (< 4%), intermediate- (4-12%), and high-risk (> 12%) groups. The ADHERE and GWTG-HF risk scores were also calculated. RESULTS: There was a significant difference in the incidence of cardiac death among the three groups stratified using the 2-year cardiac mortality risk model (p < 0.0001). The 2-year cardiac mortality risk model had a higher C-statistic (0.732) for the prediction of cardiac mortality than the ADHERE and GWTG-HF risk scores. CONCLUSION: The 2-year MIBG-based cardiac mortality risk model is useful for predicting post-discharge clinical outcomes in patients with ADHF. TRIAL REGISTRATION NUMBER: UMIN000015246, 25 September 2014.

[Successful maintenance hemodialysis therapy with supplemented growth hormone in a diabetic patient with growth hormone insufficiency].

Growth hormone (GH) insufficiency is difficult to identify especially in adults, because its clinical manifestations overlap with metabolic syndrome and diabetes mellitus. We experienced a case of a 38-year-old woman who abruptly gained weight from the age of five, and was diagnosed as type 2 diabetes mellitus (DM) during her 20s. When the patient visited JA Toride Medical Center at age 38, her renal function had been severely damaged, and caused congestive heart failure. Hemodialysis (HD) therapy was introduced, and GH insufficiency was identified, based on her obesity profile since her childhood and hormone surveillance. GH supplementation was initially avoided, because of her concurrent problems of DM and advanced renal failure. However, because of her restricted activities in daily living (ADL) and frequent hypotension episodes, a decision was taken to start supplementary administration of GH, which consequently succeeded in stabilizing blood pressure and extended her ADL. Although GH supplementation has recently been reported to be effective in improving protein energy malnutrition in dialysis patients without GH insufficiency, there is no report concerning GH insufficiency in dialysis patients. This is the first case report of GH insufficiency, in which GH supplementation enabled the patient to continue HD.

Does a proton pump inhibitor cause hypokalemia?

Proton pump inhibitors (PPIs) act only in the stomach, although the proton pump, H(+),K(+)-ATPase exists and contributes to H(+) and K(+) homeostasis in the kidney. We encountered two hypokalemic cases receiving omeprazole. These cases were women ages 69 and 80 years old. Their serum potassium levels decreased with accelerated urinary potassium excretion with the use of omeprazole, and recovered by potassium-supplement and the discontinuation of omeprazole. Because inhibitory effects of PPIs on H(+),K(+)-ATPase are exerted only in acidic condition, hypokalemia is not generally introduced by PPIs alone. However, in extreme alkalosis or impaired K(+)-recycling system, PPIs may cause hypokalemia unrelated to hypomagnesemia.

Successful treatment of hypertension in anuric hemodialysis patients with a direct Renin inhibitor, aliskiren.

OBJECTIVE: A direct renin-inhibitor (DRI), aliskiren, was administered to anuric patients to investigate whether it can be a new optional therapy against hypertension in hemodialysis (HD) patients. PATIENTS: The patients that received aliskiren comprised 8 males and 2 females with a mean ± SD age of 63 ± 8 years (43-72 years). They were exposed to dialysis therapy for 118 ± 73 months (8-251 months), with diabetes mellitus in 4 cases, chronic glomerulonephritis in 4 cases, and other diagnoses in 2 cases. METHODS: After the plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were measured before an HD session, aliskiren, 150 mg as an initial dose, was administered to the patients. PRA and PAC were also examined a week after initiating aliskiren. The blood pressure (BP) levels at the start of each HD session for a period of 2 weeks (6 HD sessions) were compared between before and after administration of aliskiren. The change of doses in other antihypertensive agents was also counted. RESULTS: The averaged reduction of mean blood pressure was 4 ± 5 mmHg, and doses of antihypertensives other than aliskiren were reduced in 4 patients. Of the examined parameters, only the reduction rate of PRA x PAC seemed correlated with the BP lowering effect of aliskiren, which was calculated as the sum of the mean BP reduction in mmHg and drug reduction with 1 tablet (capsule)/day considered to be 10 mmHg. CONCLUSION: A DRI, aliskiren, was effective even in anuric dialysis patients, and monitoring of PRA and PAC was valuable for selecting cases responsive to aliskiren.

Measurement of glomerular filtration rate by rapid intravenous injection of a newly developed inulin fraction.

OBJECTIVE: Since the conventional drip-infusion method for measuring inulin clearance (Cin) has problems related to its accuracy and performance, we explored a more accurate and concise method by rapid intravenous injection of a newly developed inulin fraction (Inulead(®)), in which spot urine sampling was omitted and the administration period of inulin was shortened from 120 to 5 minutes. PATIENTS AND METHODS: Twenty seven patients (M/F: 15/12, 67.8 ± 12.9 years old) admitted to the Nephrology ward were enrolled in this study. Inulead(®), 1500 mg dissolved in 150 mL of saline, was intravenously administered in 5 minutes. Then, sequential blood samplings and urine collection were performed for 24 hours. Cins were calculated by the following three formulae: (1) a pharmacokinetic analysis using a two compartments model based on the plasma inulin concentration to determine Cin, which was the administered dose divided by the area under the curve (AUC) from 0 to ∞, (2) urinary inulin excretion divided by the AUC for 24 hours and (3) the Bayesian method using a three-point set of plasma inulin concentrations to predict the change of inulin concentration to determine Cin as in 1. These Cins were compared with levels of estimated GFR (eGFR), creatinine clearance (Ccr), serum ß2 microglobulin (ß2MG) and serum cystatin C (Cys C). RESULTS: Cins obtained by the above three methods were well correlated with each other (r. = 0.9088 (- )0.9998) and with eGFR (r. = 0.8286 - 0.8650), Ccr (r. = 0.821 - 0.864), 1/ß2MG (r. = 0.631 - 0.752) and 1/CysC (r. = 0.830 - 0.857). The averaged differences of each Cin from eGFR were distributed between - 4.4 and - 4.5 mL/min. CONCLUSION: Since the Cins by rapid inulin injection showed satisfactory correlation and differences with other GFR parameters, this method will be a good alternative to the drip infusion method, and may reduce the burden of patients and medical staff.