Kidney Function

Background: Evaluating the accuracy of estimated glomerular filtration rate (eGFR) derived from serum creatinine (SCr) and serum cystatin C (SCysC) equations requires gold-standard measures of GFR. However, the influence of imprecise measured GFRs (mGFRs) on estimates of equation error is unknown.Study Design: Diagnostic test study.Setting & Participants: 1,995 participants from the Modification of Diet in Renal Disease (MDRD) Study and African American Study of Kidney Disease and Hypertension (AASK) with at least 2 baseline mGFRs from iodine 125–iothalamate urinary clearances, 1 standardized SCr value, and 1 SCysC value.Index Tests: eGFRs calculated using the 4-variable isotope-dilution mass spectrometry (IDMS)-traceable MDRD Study equation, the Chronic Kidney Disease (CKD) Epidemiology Collaboration (CKD-EPI) SCysC equation, the CKD-EPI SCr-SCysC equation, and mGFRs collected from another prerandomization visit.Reference Tests: A single reference mGFR, average of 2, and average of 3 mGFRs; additional analysis limited to consistent mGFRs (difference ≤25% from reference mGFR).Results: We found that mGFRs had stable mean values, but substantial variability across visits. Of all mGFRs collected a mean of 62 days apart from the reference visit, 8.0% were outside 30% of the single reference mGFR (1 − P30). Estimation equations were less accurate because 12.1%, 17.1%, and 8.3% of eGFRs from the MDRD Study, CKD-EPI SCysC, and CKD-EPI SCr-SCysC equations were outside 30% of the same gold standard (1 − P30). However, improving the precision of the reference test from a single mGFR to the average of 3 consistent mGFRs decreased these error estimates (1 − P30) to 8.0%, 12.5%, and 3.9%, respectively.Limitations: Study population limited to those with CKD.Conclusions: Imprecision in gold-standard measures of GFR contribute to an appreciable proportion of the cases in which eGFR and mGFR differ by >30%. Reducing and quantifying errors in gold-standard measurements of GFR is critical to fully estimating the accuracy of GFR estimates.

Background: Several reports have found that chronic kidney disease (CKD) is an independent risk factor for stroke. However, little is known about whether cerebrovascular disease conversely predicts the outcome of kidney function. In view of the similarities between vascular beds of the kidney and brain, we hypothesized that silent brain infarction (SBI) could reflect the degree of injury in renal small vessels and predict the risk of progression of kidney disease.Study Design: Prospective cohort study.Setting & Participants: 142 patients with CKD (stages 3-5) admitted to our clinic for education about CKD from January 2006 to July 2007 were recruited and followed up for 2 years.Predictor: SBI.Outcomes: Composite primary outcomes: doubling of serum creatinine level, development of end-stage renal disease defined as dialysis or transplant, and death from cardiovascular causes. Secondary outcome: rate of decrease in estimated glomerular filtration rate.Measurements: Brain magnetic resonance imaging was performed to determine the presence or absence of SBI.Results: At baseline, 87 patients had SBI. During follow-up, 43 patients (30.3%) developed the following primary outcomes: doubling of serum creatinine level (8 patients), dialysis therapy (32 patients), and death from cardiovascular causes (3 patients). In crude analysis, the presence of SBI predicted time to primary outcomes (P = 0.01). A multivariate Cox model confirmed the presence of SBI to be an independent predictor of study outcomes (HR, 2.16; 95% CI, 1.01-4.64; P = 0.04). Estimated glomerular filtration rate decreased more in patients with SBI than in those without SBI (−0.11/y vs −0.06/y relative to baseline value; P = 0.005).Limitations: Study size was small.Conclusion: We showed that SBI was an important independent prognostic factor for the progression of kidney disease in patients with CKD. Our findings suggest that patients with SBI should be considered a high-risk population for decreased kidney function.

We report a case of Churg-Strauss syndrome coexistent with coronary vasospasm and pauci-immune necrotizing crescentic glomerulonephritis. A 54-year-old man with bronchial asthma and allergic rhinitis was admitted to our hospital because of acute coronary syndrome. Angiography showed diffuse coronary artery spasm without anatomic stenosis. Acute coronary syndrome due to vasospasm was diagnosed. However, subsequent administration of vasodilators did not suppress angina symptoms. In addition, marked eosinophilia, eosinophilic pneumonitis, chronic sinusitis, pericardial effusion, and slight hematuria with red blood cell casts were detected. Although kidney function was normal, a kidney biopsy showed necrotizing crescentic glomerulonephritis with eosinophilic infiltration in both glomeruli and interstitium. With the diagnosis of Churg-Strauss syndrome, oral prednisolone at a dose of 60 mg/d was administered. Cardiac symptoms, pulmonary and sinonasal lesions, pericardial effusion, and urine sediment resolved rapidly. Six months later, a repeated kidney biopsy showed remarkable improvement and no eosinophilic infiltration. Coronary vasospasm with eosinophilia might be refractory to vasodilators and sensitive to corticosteroid therapy and often has been related to Churg-Strauss syndrome. Slight abnormalities in urine sediment can be the clue to the diagnosis of severe kidney involvement of Churg-Strauss syndrome.