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Renal Papillary Necrosis in Patients with Sickle Cell Trait: A Fifteen Year Single Institution Descriptive Case Series
Leon Chertin, MD, Kohl Killeen, MD, Richard A. Brown, BS, Jessica Makram, BS, Mohamed Soltan, MD, Dana W. Giel, MD, Mary E. Killian, MD, EMBA.
University of Tennessee Health Science Center, Memphis, TN, USA.
BACKGROUND: Sickle cell trait (SCT), the heterozygous carrier state for hemoglobin S, has historically been regarded as benign. However, the renal medulla is uniquely susceptible to sickling-induced ischemia even in heterozygous carriers, due to its hypoxic, hyperosmolar, and acidic microenvironment. Renal papillary necrosis (RPN), a recognized complication of sickle cell disease, has been described in SCT primarily through isolated case reports. Large pediatric series are lacking. This study presents a 15-year institutional experience characterizing the prevalence, clinical presentation, and laboratory profile of RPN in a pediatric SCT cohort.
METHODS: A retrospective descriptive case series was conducted at a single pediatric tertiary care center over a 15-year period. Medical records of pediatric patients with confirmed SCT were reviewed. Clinical, laboratory, and medication variables were compared between patients with and without RPN. The observed RPN prevalence was compared to an estimated background population rate.
RESULTS: Of 251 pediatric SCT patients, 7 (2.79%; 95% CI 1.13%-5.66%) had confirmed RPN, a rate significantly higher than the estimated 0.1% background rate in the general pediatric population, where RPN occurs predominantly in adults over 40 years of age (p < 0.001). Gross hematuria was the most discriminating clinical feature, present in 86% of RPN cases compared to 9.5% of non-RPN patients (p < 0.001). Transfusion therapy was more frequent in the RPN group (57% vs. 17%, p = 0.021). Kidney failure was documented in 29% of RPN patients, all classified as Stage 4, compared to 7% in the non-RPN group. NSAID use was borderline significant (43% vs. 12%, p = 0.050), consistent with prior reports linking analgesic exposure to papillary ischemia in SCT carriers. Proteinuria, microscopic hematuria, and pyuria were each present in 86% of RPN cases. Nitrite positivity was absent in all RPN cases, supporting an ischemic rather than infectious etiology. Renal function markers and inflammatory markers did not differ significantly between groups. No cases of renal medullary carcinoma were identified, though it was evaluated given its known association with SCT. Demographic characteristics including sex, race, and insurance status did not differ significantly between groups.
CONCLUSIONS: RPN occurs at a markedly elevated rate in pediatric SCT patients compared to the general population. Gross hematuria should prompt consideration of RPN and renal imaging in this population. NSAID exposure warrants caution in SCT carriers. These findings challenge the notion that SCT is uniformly benign and highlight the need for early recognition and nephroprotective management in affected children.
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