Urinary excretion of ß2-microglobulin as a prognostic marker in immunoglobulin A nephropathy.

BACKGROUND/AIMS: ß2-microglobulin (ß2-MG) is freely filtered at the glomerulus and subsequently reabsorbed and catabolized by proximal renal tubular cells. Urinary ß2-MG is an early and sensitive biomarker of acute kidney injury; however, its utility as a biomarker of immunoglobulin A nephropathy (IgAN) is unclear. METHODS: We included urinary ß2-MG levels in the routine laboratory examination of all inpatients with biopsy-proven IgAN at our hospital from 2006 to 2010. We retrospectively analyzed the correlation between ß2-MG levels and clinical parameters as a prognostic biomarker of IgAN. RESULTS: A total of 51 patients (30 males, 21 females; mean age, 33.01 ± 12.73 years) with IgAN were included in this study. Initial demographic, clinical, and laboratory data for all patients are listed. The mean initial estimated glomerular filtration rate and 24-hour urine protein levels were 94.69 ± 34.78 mL/min/1.73 m(2) and 1.28 ± 1.75 g/day, respectively. The mean level of urinary ß2-MG was 1.92 ± 7.38 µg/mg creatinine. There was a significant correlation between initial serum creatinine (iSCr), urine protein creatinine ratio (UPCR), and the level of ß2-MG (r = 0.744, r = 0.667, p < 0.01). There was also a significant correlation between renal function tests and the level of urinary ß2-MG (p < 0.01). Cox regression analysis showed that albumin, ß2-MG, iSCr, and UPCR were significant predictors of disease progression in IgAN. CONCLUSIONS: Urinary ß2-MG levels showed a significant correlation with renal function and proteinuria in IgAN. Thus, we propose that urinary ß2-MG may be an additional prognostic factor in patients with IgAN.

A case of possible neurosarcoidosis presenting as intractable headache and panhypopituitarism.

Sarcoidosis is a chronic multisystemic inflammatory disease of unknown etiology, which is characterized by noncaseating granulomatous inflammation of the involved organs. It is known that neurosarcoidosis involving the nervous system occurs in about 5% of patients with sarcoidosis. However, neurosarcoidosis without systemic involvement is extremely rare. We present a case of suspicious neurosarcoidosis affecting the pituitary gland, which was manifested as chronic uncontrolled headache, panhypopituitarism, central diabetes insipidus, and hypercalcemia. Though the biopsy at the pituitary lesion was not performed due to the high risk of surgical complication, treatment was needed urgently and we started steroid therapy. After steroid therapy, we observed the immediate symptom relief with improved hypercalcemia. According to the follow-up examination, no recurrent symptom was seen, and resolution of the pituitary lesion with improving panhypopituitarism was noted.

Severe Hyponatremia Associated with the Use of Angiotensin II Receptor Blocker/thiazide Combinations.

There are several widely used combinations of angiotensin II receptor blocker (ARB)/thiazide. The complimentary mechanism of action for such anti-hypertensive therapies is that, while ARB inhibits the vasoconstricting and aldosterone-secreting effects of angiotensin II, hydrochlorothiazide affects the renal tubular mechanisms of electrolyte reabsorption and increases excretion of sodium and chloride in the distal tubule, consequently promoting water excretion. In addition, hypokalemia, which may be triggered by a hydrochlorothiazide-induced increase in urinary potassium loss, is resisted by the use of ARB. Hence, the ARB/thiazide combination is safe in terms of potassium imbalance. For these reasons, fixed-dose ARB/thiazide combination anti-hypertensive drugs have been widely used for the treatment of hypertension. However, there have not been many studies done regarding cases where patients under such regimens showed severe hyponatremia, even when the amount of thiazide included was low. Here we report two cases in which severe hyponatremia occurred following treatment with the ARB/thiazide combinations. Upon discontinuation of the regimen, both patients showed recovery from hyponatremia.

Relationship between glomerulomegaly and clinicopathologic findings in IgA nephropathy.

BACKGROUND: Large glomeruli are a common finding in the early stages of progressive renal disease. We studied the relationship between glomerular surface area (GSA) and clinicopathologic features of IgA nephropathy (IgAN), including renal outcome, to better understand the role of GSA in IgAN. METHODS: We analyzed renal biopsy specimens and clinical information from 34 patients with IgAN. Mean and maximal GSA were determined using a computed imaging analyzer. RESULTS: Mean GSA was 16,811 ± 4,671 µ2 in IgAN patients (n = 34). When we analyzed various clinical parameters of IgAN patients, there were significant correlations between mean or maximal GSA and age, body mass index (BMI), systolic and diastolic blood pressure, estimated glomerular filtration rate (eGFR), and pathologic findings including H.S. Lee' grades, interstitial fibrosis, and tubular atrophy. GSA did not show any relationship with the degree of hematuria and proteinuria. By multivariate regression analysis of age, BMI, blood pressure, H.S. Lee' grades, and eGFR as independent variables, mean GSA was associated with H.S Lee' grades and initial eGFR. The results for maximal GSA were the same as those for mean GSA. When we divided IgAN patients according to their mean levels of GSA, the group with larger GSA had higher blood pressure and H.S. Lee' grades and lower initial and final eGFR. More patients in the larger GSA group showed the decline in eGFR of more than 15 ml/min/1.73 m2 during the followup period compared with the smaller group. CONCLUSION: These results suggest that glomerular size, estimated by measuring GSA, is related to pathologic findings and renal function in IgAN. However, further investigation is required to determine if GSA can be used as a prognostic indicator of IgAN.

Etiology of hypokalemic paralysis in Korea: data from a single center.

Recognizing the underlying causes of hypokalemic paralysis seems to be essential for the appropriate management of affected patients and their prevention of recurrent attacks. There is, however, a paucity of documented reports on the etiology of hypokalemic paralysis in Korea. We retrospectively analyzed 34 patients with acute flaccid weakness due to hypokalaemia who were admitted during the 5-year study period in order to determine the spectrum of hypokalemic paralysis in Korea and to identify the differences in clinical parameters all across the causes of hypokalemic paralysis. We divided those 34 patients into 3 groups; the 1(st) group, idiopathic hypokalemic periodic paralysis (HPP), the 2(nd), thyrotoxic periodic paralysis (TPP), and the 3rd group, secondary hypokalemic paralysis (HP) without TPP. Seven of the patients (20.6%) were diagnosed as idiopathic HPP considered the sporadic form, and 27 patients (79.4%) as secondary HP. Among the patients diagnosed as secondary HP, 16 patients (47.1%) had TPP. Patients of secondary hypokalemic paralysis without TPP required a longer recovery time compared with those who had either idiopathic HPP or TPP. This is due to the fact that patients of secondary HP had a significantly negative total body potassium balance, whereas idiopathic HPP and TPP were only associated with intracellular shift of potassium. Most of the TPP patients included in our study had overt thyrotoxicosis while 3 patients had subclinical thyrotoxicosis. This study shows that TPP is the most common cause of hypokalemic paralysis in Korea. And we suggest that doctors should consider the presence of TPP in patients of hypokalemic paralysis even if they clinically appear to be euthyroid state.