Cardiac valve calcification is associated with the presence and severity of CAD in pre-dialysis CKD. Assessment of cardiac valve calcification by means of transthoracic echocardiography could be a valuable non-invasive method for CAD risk stratification in pre-dialysis CKD patients.

BackgroundStress-induced cardiomyopathy (sCMP) is characterized by transient wall-motion abnormalities involving the left ventricular apex and mid-ventricle that are precipitated by emotional or physical stress. As the heart and kidney influence each other’s function through bidirectional pathways, sCMP can induce renal dysfunction or be induced by renal dysfunction. This study reviewed the clinical characteristics and outcomes of patients with confirmed sCMP associated with renal dysfunction.MethodsWe conducted a retrospective analysis of the medical records of all patients from our institution who were diagnosed with sCMP from March 2010 to April 2012. Each patient’s demographic characteristics, presenting symptoms, triggering events, electrocardiographic characteristics, laboratory data, echocardiographic study findings, cardiac catheterization data, and outcomes were reviewed.ResultsAmong 30 patients who were diagnosed with sCMP, 7 patients had associated renal dysfunction. Three patients were on maintenance hemodialysis (HD) and 4 patients had acute kidney injury (AKI). Their mean ejection fraction was 35.2% at initial echocardiography, and 57.2% at follow-up echocardiography. Pericardial effusion was detected in all HD patients initially; these patients were treated with intensive HD for suspected under-dialysis status. In patients with AKI, the mean peak serum creatinine was 4.17 mg/dL. Two patients were treated with continuous renal replacement therapy. One patient required maintenance HD, and 1 patient died. Two patients had full renal recovery to their baseline renal function at 7 and 14 days.ConclusionsPatients with renal dysfunction including those with AKI and those undergoing HD can develop sCMP, renal function must be closely monitored in patients with sCMP. Additionally, it should be considered that patients on HD who develop sCMP may be under-dialyzed.

5-Lipoxygenase inhibitor and human recombinant erythropoietin might accelerate renal recovery in cisplatin-induced acute renal failure rats. Male Sprague-Dawley rats were randomized into four groups: 1) normal controls; 2) Cisplatin group-cisplatin induced acute renal failure (ARF) plus vehicle treatment; 3) Cisplatin+nordihydroguaiaretic acid (NDGA) group-cisplatin induced ARF plus 5-lipoxygenase inhibitor treatment; 4) Cisplatin+erythropoietin (EPO) group-cisplatin induced ARF plus erythropoietin treatment. On day 10 (after 7 daily injections of NDGA or EPO), urea nitrogen and serum Cr concentrations were significantly lower in the Cisplatin+NDGA and Cisplatin+EPO groups than in the Cisplatin group, and 24 hr urine Cr clearances were significantly higher in the Cisplatin+EPO group than in the Cisplatin group. Semi-quantitative assessments of histological lesions did not produce any significant differences between the three treatment groups. Numbers of PCNA(+) cells were significantly higher in Cisplatin, Cisplatin+NDGA, and Cisplatin+EPO groups than in normal controls. Those PCNA(+) cells were significantly increased in Cisplatin+NDGA group. These results suggest that EPO and also NDGA accelerate renal function recovery by stimulating tubular epithelial cell regeneration.

A 74-yr-old woman presented with fever and abdominal discomfort. She was in a septic condition caused by urinary tract infection. Her computed tomogram of the abdomen revealed features of hydronephrosis with ureteral stones in both kidneys. During percutaneous nephrostomies, right pyeloduodenal fistula (PDF) was diagnosed. Elective surgery was originally planned but the patient was in a poor condition to undergo surgery. Instead, 2 times endoscopic clipping and ligation by endoloop were applied with parenteral antibiotics for the fistula lesion. On admission day 30, she was discharged from the hospital after confirmation of no more contrast leakage on fistulography. We reviewed the literature and discuss the etiologies, clinical presentations, diagnosis, and treatment of PDF.