Serum klotho levels in acute kidney injury
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AIMS: Klotho is a co-receptor for FGF-23 and key regulator of phosphate excretion. Soluble klotho modulates ion-channel expression and growth factor sensitivity. In chronic kidney disease (CKD), impaired klotho expression has been demonstrated. Likewise, reduced soluble klotho levels in serum and urine have been established in rodents in experimental acute kidney injury (AKI). In contrast, no data on soluble serum klotho levels in human AKI has been presented to date. MATERIAL AND METHODS: A cross-sectional case-control study of klotho serum levels in 30 subjects with AKI and 126 control subjects with kidney functions ranging from normal to end-stage renal disease (ESRD). RESULTS: Klotho levels were higher in AKI patients (567.6 ± 294.4 pg/mL, vs. 403.5 ± 152.5 pg/mL, p < 0.01) and females (463.0 ± 202.6 pg/mL vs. 387.6 ± 132.0 pg/mL, p < 0.01) and lower in ESRD patients than in healthy adults and patients with moderate CKD (368.3 ± 99.0 pg/mL vs. 468.1 ± 205.8, p < 0.01 and 368.3 ± 99.0 pg/mL vs. 498.7 ± 221.9, p < 0.01). There was a correlation with estimated glomerular filtration rate (eGFR) in CKD (p < 0.0001, r = 0.34). CONCLUSIONS: In AKI, serum klotho levels are not associated with kidney function whereas in CKD, impaired klotho levels may be observed and are significantly correlated to eGFR.
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Oliguric acute kidney injury as a main symptom of bradycardia and arteriosclerosis resolved by pacemaker implantation: a case report.

INTRODUCTION: Cardiovascular comorbidities regularly determine renal function. We report a case of acute kidney injury (Acute Kidney Injury Network stage 3) due to an intermittent third-degree atrioventricular block, which had not been diagnosed before. CASE PRESENTATION: A 76-year-old Caucasian man with liver cirrhosis due to non-alcoholic fatty liver disease, and type-2 diabetes was cognitively impaired and had reduced vigilance presumably caused by hepatic encephalopathy and/or Alzheimer dementia. Within 2 years, two hospitalizations occurred for syncope attributed to orthostatic failure and hypovolemia. During the last hospitalization, oliguric acute kidney injury occurred. Sonography ruled out a post-renal cause. His renal resistive index was 1.0; his heart rate was below 50 beats per minute. After cessation of beta-blocker therapy, Holter electrocardiogram showed a new intermittent third-degree atrioventricular block with pauses for less than 3 seconds. Pacemaker insertion resolved his acute kidney injury, despite resumption of beta-blocker therapy. During four months of follow-up, syncope has not occurred, and vigilance was stable. However, his renal resistive index of 1.0 remained. CONCLUSIONS: Here, typical neurologic symptoms of bradycardia were misclassified. Diagnostic work-up of oliguric acute kidney injury revealed intermittent third-degree heart block. The pathomechanism of acute kidney injury relates to relevant bradycardia and increased vascular stiffness attenuating arterial diastolic renal blood flow.