BACKGROUND: Chronic kidney disease (CKD) is a growing problem among the elderly. Early detection is considered essential to ensure proper treatment and to avoid drug toxicity, but detection is challenging because elderly patients with CKD often have normal serum creatinine levels. We hypothesized that most cases of CKD in the elderly would go undetected, resulting in inappropriate prescribing. OBJECTIVE:To determine whether recognition of CKD is associated with more appropriate treatment DESIGN: Retrospective chart review PARTICIPANTS: All patients aged ≥65 years with a measured serum creatinine in the past 3 years at 2 inner city academic health centers.MEASUREMENTS: Estimated glomerular filtration rate (eGFR) calculated using the Modified Diet in Renal Disease equation, and for patients with eGFR<60, documentation of CKD by the provider, diagnostic testing, nephrology referral and prescription of appropriate or contraindicated medications. RESULTS:Of 814 patients with sufficient information to estimate eGFR, 192 (33%) had moderate (eGFR< 60 mL/min) and 5% had severe (eGFR<30 mL/min) CKD. Providers identified 38% of moderate and 87% of severe CKD. Compared to patients without recognized CKD, recognized patients were more likely to receive an ACE/ARB (80% vs 61%, p=.001), a nephrology referral (58% vs 2%, p<.0001), or urine testing (75% vs 47%, p<.0001), and less likely to receive contraindicated medications (26% vs 40%, p=.013). CONCLUSIONS:Physicians frequently fail to diagnose CKD in the elderly, leading to inappropriate treatment. Efforts should focus on helping physicians better identify patients with low GFR.

Background-Long-QT (LQT) syndrome is a cardiac disorder that causes syncope, seizures, and sudden death from ventricular arrhythmias, specifically torsade de pointes. Both autosomal dominant LQT (Romano-Ward syndrome) and autosomal recessive LQT (Jervell and Lange-Nielsen syndrome, JLNS) have been reported. Heterozygous mutations in 3 potassium channel genes, KVLQT1, KCNE1 (minK), and HERG, and the cardiac sodium channel gene SCN5A cause autosomal dominant LQT. Autosomal recessive LQT, which is associated with deafness, has been found to occur with homozygous mutations in KVLQT1 and KCNE1 in JLNS families in which QTc prolongation was inherited as a dominant trait. Methods and Results-An Amish family with clinical evidence of JLNS was analyzed for mutations by use of single-strand conformation polymorphism and DNA sequencing analyses for mutations in all known LQT genes. A novel homozygous 2-bp deletion in the S2 transmembrane segment of KVLQT1 was identified in affected members of this Amish family in which both QTc prolongation and deafness were inherited as recessive traits. This deletion represents a new JLNS-associated mutation in KVLQT1 and has deleterious effects on the KVLQT1 potassium channel, causing a frameshift and the truncation of the KVLQT1 protein. In contrast to previous reports in which LQT was inherited as a clear dominant trait, 2 parents in the JLNS family described here have normal QTc intervals (0.43 and 0.44 seconds, respectively). Conclusions-A novel homozygous KVLQT1 mutation causes JLNS in an Amish family with deafness that is inherited as an autosomal recessive trait. (Circulation. 1999;99:1344-1347.)