ABSTRACT
BACKGROUND: Chronic smoking and hypertension may lead to smoking-related nodular glomerulopathy (SRNG), a well-recognized entity that clinically and pathologically mimics nodular diabetic nephropathy (DN). However, like DN, diffuse mesangial sclerosis may occur in this setting without nodules. METHODS: The clinicopathologic features of 10 non-diabetic patients with a long smoking history diagnosed from 2003-2012 showing diffuse mesangial glomerulosclerosis (6) or SRNG (4) were analyzed. RESULTS: Nine of 10 patients were men, aged 58-80 with a 20-58 pack-year smoking history. None of the patients manifested diabetes, but all of them had hypertension. Numerous other cardiovascular comorbidities were present. At biopsy, the mean creatinine was 1.9 mg/dl (range 1.4-3) and the mean proteinuria was 3.9 g/24 h. The renal pathologic findings were similar in all patients except mesangial nodules in SRNG. Global glomerulosclerosis was seen in 6-72% of glomeruli (mean 31%), glomerulomegaly in all cases, and a range of interstitial fibrosis in 10-70% (mean 43%). Moderate (40%) and severe (50%) arteriosclerosis and arteriolar hyalinosis (80%) were also observed. Glomerular hilar or mesangial neovascularization was prominent. Endothelial swelling, subendothelial widening, and new basement membrane formation suggesting chronic healing thrombotic microangiopathy (TMA) was noted in 80%. No immune complexes were localized. CONCLUSIONS: Kidney biopsies from patients with proteinuria and chronic renal insufficiency in the setting of prolonged smoking and hypertension show either diffuse or nodular mesangial glomerulosclerosis. Chronic glomerular mesangial and endothelial injury associated with smoking leads to a chronic TMA appearance in the appropriate setting, even in the absence of mesangial nodule formation.
Subject(s)
Nephrotic Syndrome/etiology , Nephrotic Syndrome/pathology , Sclerosis/etiology , Sclerosis/pathology , Smoking/adverse effects , Aged , Aged, 80 and over , Arterioles , Arteriosclerosis/pathology , Creatinine/blood , Diarrhea/pathology , Eye Diseases, Hereditary/pathology , Female , Fibrosis/pathology , Glomerular Basement Membrane/pathology , Glomerulosclerosis, Focal Segmental/pathology , Humans , Hypertension/complications , Intestinal Diseases/pathology , Male , Middle Aged , Neovascularization, Pathologic/pathology , Proteinuria/urine , Skin Abnormalities/pathology , Thrombotic Microangiopathies/pathology , Vascular Diseases/pathologyABSTRACT
OBJECTIVE: Several studies have confirmed the remarkable observation that cumulative urinary potassium (K(+)) excretion is less in African-Americans than White Americans even when identical amounts of potassium are provided in the diet. This study was designed to examine whether this decrease in urinary potassium could be compensatory to an increase in gastrointestinal excretion of potassium in African-Americans. METHODS: Twenty-three young, healthy, normotensive participants of both sexes and races were placed on a fixed diet of 100 mEq per day of K(+) and 180 mEq per day of sodium (Na(+)) for 9 days. All urine and stool were collected daily and analyzed for electrolytes. Blood was obtained for determination of electrolytes, blood urea nitrogen (BUN), creatinine, glucose, insulin, renin, and aldosterone at the beginning and at the end of the study period. RESULTS: Cumulative urinary excretion of K(+) was significantly less in African-Americans (609 ± 31 mEq) compared with White Americans (713 ± 22 mEq, P = 0.015). There was no significant racial difference, however, in the cumulative gastrointestinal excretion of K (105 ± 11 versus 95 ± 9 mEq, P = 0.28) in African-Americans versus White Americans, respectively. CONCLUSION: The racial difference in urinary K(+) handling manifested by decreased excretion of K(+) in African-Americans cannot be attributed to an increase in net gastrointestinal excretion of this cation.
