Unresolved subclinical hypothyroidism is independently associated with progression of chronic kidney disease.

BACKGROUND AND AIM: Patients with chronic kidney disease (CKD) often have subclinical hypothyroidism. However, few reports have investigated changes in the status of subclinical hypothyroidism in CKD patients and its clinical significance in CKD progression. METHODS: We included 168 patients with nondialysis-dependent CKD stages 2-4. The normalization of subclinical hypothyroidism during follow-up was assessed, and the association between transitions in subclinical hypothyroid status and the rate of decline of the estimated glomerular filtration rate (eGFR) was investigated. RESULTS: At baseline, 127 patients were euthyroid and 41 (24.4%) patients were diagnosed with subclinical hypothyroidism. Of these 41 patients, 21 (51.2%) spontaneously resolved to euthyroid during follow-up. The rate of eGFR decline of patients with resolved subclinical hypothyroidism was similar to that of euthyroid patients. The patients with unresolved subclinical hypothyroidism showed a steeper renal function decline than patients with euthyroidism or resolved subclinical hypothyroidism (all p < 0.05). The progression to end-stage renal disease was more frequent in those with unresolved subclinical hypothyroidism than in those who were euthyroid (p = 0.006). In multivariate linear regression for rate of eGFR decrease, unresolved subclinical hypothyroidism (ß = -5.77, p = 0.001), baseline renal function (ß = -0.12, p < 0.001) and level of proteinuria (ß = -2.36, p = 0.015) were independently associated with the rate of renal function decline. CONCLUSIONS: Half of the CKD patients with subclinical hypothyroidism did not resolve to euthyroidism, and this lack of resolution was independently associated with rapid renal function decline.

Rifampin-associated tubulointersititial nephritis and Fanconi syndrome presenting as hypokalemic paralysis.

BACKGROUND: Rifampin is one of the most important drugs in first-line therapies for tuberculosis. The renal toxicity of rifampin has been reported sporadically and acute tubulointerstitial nephritis (ATIN) is a frequent histological finding. We describe for the first time a case of ATIN and Fanconi syndrome presenting as hypokalemic paralysis, associated with the use of rifampin. CASE PRESENTATION: A 42-year-old man was admitted with sudden-onset lower extremity paralysis and mild renal insufficiency. He had been treated for pulmonary tuberculosis with isoniazid, rifampin, and ethambutol for 2 months. Laboratory tests revealed proteinuria, profound hypokalemia, hyperchloremic metabolic acidosis with a normal anion gap, positive urine anion gap, hypophosphatemia with hyperphosphaturia, hypouricemia with hyperuricosuria, glycosuria with normal serum glucose level, generalized aminoaciduria, and ß2-microglobulinuria. A kidney biopsy revealed findings typical of ATIN and focal granular deposits of immunoglubulin A and complement 3 in the glomeruli and tubules. Electron microscopy showed epithelial foot process effacement and electron-dense deposits in the subendothelial and mesangial spaces. Cessation of rifampin resolved the patient's clinical presentation of Fanconi syndrome, and improved his renal function and proteinuria. CONCLUSION: This case demonstrates that rifampin therapy can be associated with Fanconi syndrome presenting as hypokalemic paralysis, which is a manifestation of ATIN. Kidney function and the markers of proximal tubular injury should be carefully monitored in patients receiving rifampin.

Decisive indicator for gastrointestinal workup in anemic patients with nondialysis chronic kidney disease.

BACKGROUND: Anemia and iron deficiency are universal problems in patients with chronic kidney disease (CKD). However, decisive indicator to guide the further gastrointestinal (GI) workup has not been determined. METHODS: We included 104 anemic patients with nondialysis-dependent CKD stages 3-5 (38 patients at stage 3, 26 patients at stage 4, and 40 patients at stage 5). Hemoglobin, serum ferritin, transferrin saturation (TSAT), mean corpuscular volume (MCV), and corrected reticulocyte count data were assessed to evaluate diagnostic utility for bleeding-related GI lesions, which were identified by esophagogastroduodenoscopy and colonoscopy. RESULTS: Bleeding-related GI lesions were found in 55 (52.9%) patients, and patients with stage 5 CKD had a higher prevalence of gastric lesions than patients with CKD stage 3 or 4 (all p < 0.05). The areas under the receiver operating characteristic curves used to predict bleeding-related lesions were 0.69 for TSAT (p = 0.002) and 0.61 for serum ferritin (p = 0.085). The sensitivity and specificity of a cutoff value for TSAT < 20% were 0.59 and 0.74, respectively. Hemoglobin, MCV, and corrected reticulocyte levels had no significant diagnostic utility. On multivariable logistic regression, the chance of GI lesions increased by 6% for each 1% reduction in TSAT and increased 4.1-fold for patients with CKD stage 5 (all p < 0.05). CONCLUSIONS: TSAT is a useful indicator for determining the GI workup in anemic patients with nondialysis-dependent CKD stages 3-5. Stage 5 CKD is independently associated with bleeding-related lesions and TSAT should be used cautiously in these patients.

Use of blood tests to predict upper gastrointestinal lesions in patients with chronic kidney disease.

OBJECTIVE: Anemia and iron deficiency are common complications in patients with chronic kidney disease (CKD). However, information about the diagnostic indicators of bleeding-related upper gastrointestinal (GI) tract lesions is sparse and few studies have investigated anemic upper GI tract lesions. METHODS: We included 165 anemic patients with non-dialysis-dependent CKD stages 3 to 5 (44 patients at stage 3, 52 patients at stage 4, and 69 patients at stage 5). Transferrin saturation (TSAT), serum ferritin, mean corpuscular volume, and corrected reticulocyte count data were collected to evaluate their diagnostic use for bleeding-related upper GI tract lesions, which were identified by esophagogastroduodenoscopy. RESULTS: Bleeding-related GI tract lesions were found in 57 patients (34.5%). The area under the receiver-operating characteristic curve used to predict bleeding-related lesions was 0.63 for TSAT (P = 0.007), and the best cutoff value was 19.7% (sensitivity, 0.53; specificity, 0.76). The combination of cutoffs TSAT less than 20% or serum ferritin less than 100 ng/mL produced a 17% increment in sensitivity compared with that of TSAT less than 20% alone. The corrected reticulocyte levels and mean corpuscular volume had no significant diagnostic use. In patients with CKD stage 5, the sensitivity of TSAT or its combination with serum ferritin less than 100 ng/mL was significantly lower than in patients with CKD stage 3 (all P < 0.05). CONCLUSIONS: Transferrin saturation is a significant predictor of anemic lesions in the upper GI tract, and serum ferritin can increase the sensitivity of TSAT. However, these indicators should be used with caution in patients with CKD stage 5 because their sensitivity is poor in this context.

Second primary glioblastoma multiforme following autologous hematopoietic stem cell transplantation in a patient with acute myelogenous leukemia.

Glioblastoma multiforme (GM) is one of the most aggressive primary brain tumors, and has a poor prognosis despite intensive treatment. GM is also the most malignant astrocytoma, with histopathological features that include cellular polymorphism, rapid mitotic activity, microvascular proliferation, and necrosis. The causes of GM remain obscure, but several reports have shown associations between GM and genetic alterations and radiation exposure. Furthermore, high-dose chemotherapy/radiotherapy with autologous stem cell transplantation is increasingly being used to treat patients with leukemia, and patients who undergo stem cell transplantation have a higher risk of solid tumor cancer development later in life. Based on these associations, we discuss GM development in a patient who underwent chemoradiotherapy conditioning prior to stem cell transplantation.

Stent fracture at the proximal shaft of the left main stem.

Stent fracture is likely to be caused due to mechanical stress at the hinge point or kinking movement at the point of aneurysm formation with stent malapposition. To our knowledge, this is the first published report of stent fracture at the proximal shaft of the left main stem in a patient with acute myocardial infarction.