BACKGROUND: Stem cell transplantation (SCT) places a heavy burden on the kidneys, often resulting in renal dysfunction or nephrotic syndrome. This study attempted to show that early-onset proteinuria predicts the development of overt nephropathy. METHODS: A total of 831 patients who received allogeneic SCT were surveyed. Excluding those with prior kidney disease and those lacking in an observation period ≥1 year after SCT, 251 patients were eligible for the study. Dipstick proteinuria ≥1+ within 1 year after SCT was defined as 'incident proteinuria', and subsequent persistence of an estimated glomerular filtration rate of <60 ml/min/1.73 m2 at 1 year or longer after SCT was defined as 'incident chronic kidney disease (CKD)'. Between-group differences were analyzed using the chi-square or Mann-Whitney U test. Factors associated with the incidence of CKD were investigated by multivariate Cox proportional regression analysis. Kidney-biopsied tissue was examined in all nephrotic syndrome patients. RESULTS: The mean duration of follow-up was 4 years. Thirty-four (13.5%) and 66 (26.3%) patients developed incident proteinuria and incident CKD, respectively. Nine (3.6%) patients developed nephrotic syndrome mainly due to membranous nephropathy. The incidence of CKD was significantly greater in patients with incident proteinuria than those without (61.8 vs. 20.7%, p < 0.0001), and incident dipstick proteinuria was a significant risk for incident CKD (hazard ratio 4.39, 95% CI 2.44-7.73, p < 0.0001). CONCLUSION: SCT patients who manifest dipstick proteinuria are predisposed to overt nephropathy. Routine monitoring of the urine dipstick test is strongly recommended, as it facilitates early nephrology care for post-SCT patients.
BACKGROUND: Stem cell transplantation (SCT) places a heavy burden on the kidneys, often resulting in renal dysfunction or nephrotic syndrome. This study attempted to show that early-onset proteinuria predicts the development of overt nephropathy. METHODS: A total of 831 patients who received allogeneic SCT were surveyed. Excluding those with prior kidney disease and those lacking in an observation period ≥1 year after SCT, 251 patients were eligible for the study. Dipstick proteinuria ≥1+ within 1 year after SCT was defined as 'incident proteinuria', and subsequent persistence of an estimated glomerular filtration rate of <60 ml/min/1.73 m2 at 1 year or longer after SCT was defined as 'incident chronic kidney disease (CKD)'. Between-group differences were analyzed using the chi-square or Mann-Whitney U test. Factors associated with the incidence of CKD were investigated by multivariate Cox proportional regression analysis. Kidney-biopsied tissue was examined in all nephrotic syndromepatients. RESULTS: The mean duration of follow-up was 4 years. Thirty-four (13.5%) and 66 (26.3%) patients developed incident proteinuria and incident CKD, respectively. Nine (3.6%) patients developed nephrotic syndrome mainly due to membranous nephropathy. The incidence of CKD was significantly greater in patients with incident proteinuria than those without (61.8 vs. 20.7%, p < 0.0001), and incident dipstick proteinuria was a significant risk for incident CKD (hazard ratio 4.39, 95% CI 2.44-7.73, p < 0.0001). CONCLUSION: SCT patients who manifest dipstick proteinuria are predisposed to overt nephropathy. Routine monitoring of the urine dipstick test is strongly recommended, as it facilitates early nephrology care for post-SCT patients.
Authors: Amanda DeMauro Renaghan; Edgar A Jaimes; Jolanta Malyszko; Mark A Perazella; Ben Sprangers; Mitchell Howard Rosner Journal: Clin J Am Soc Nephrol Date: 2019-12-13 Impact factor: 8.237