Jeng-Jong Huang

Decreased predominance of papG class II allele in Escherichia coli strains isolated from adults with acute pyelonephritis and urinary tract abnormalities.

PURPOSE We compared the genotypes of fimbriae or adhesions of Escherichia coli causing acute pyelonephritis in adults with and without urinary tract abnormalities. MATERIALS AND METHODS We studied a total of 92 E. coli strains isolated from 54 patients with acute pyelonephritis and a normal urinary tract, and 38 with urinary tract abnormalities. Of those with urinary tract abnormalities 13 with moderate to severe hydronephrosis were also considered a separate group for the purpose of analysis. The genes of 7 known fimbriae or adhesins of E. coli were detected by the polymerase chain reaction, including the papG class I to III alleles (PapG adhesins of P-fimbriae), sfa/foc (S-/F1C-fimbriae), fimH (type 1 fimbriae), and afa (afimbrial adhesin). Virulence genes associated with APN were identified by comparing the prevalence of each of these 7 genes in E. coli strains from 54 patients with acute pyelonephritis with a normal urinary tract to the prevalence in the strains from 37 patients with acute cystitis using univariate and multivariate analysis. Differences in the prevalence of the genes associated with acute pyelonephritis and the incidence of underlying illness were then compared in the 3 acute pyelonephritis groups. RESULTS On univariate and multivariate analysis the papG class II allele was the only virulence gene associated with acute pyelonephritis (p <0.0001 and 0.001, respectively). No significant difference was noted in the prevalence of underlying medical disease in the 3 acute pyelonephritis groups. The papG class II allele was significantly less predominant in E. coli strains isolated from acute pyelonephritis cases with versus without urinary tract abnormalities (76% versus 93%, p = 0.03). The incidence of the papG class II allele in patients with urinary tract abnormalities and moderate to severe hydronephrosis was less than in those without urinary tract abnormalities (69% versus 93%, p = 0.04). CONCLUSIONS Our results imply that the papG class II allele has an important role in E. coli infection in patients with acute pyelonephritis and a normal urinary tract, while urinary tract abnormalities and/or obstruction may permit ascending infection of E. coli strains with lower adhesive ability.

Clinical features of thin basement membrane disease and associated glomerulopathies.

Background:  Thin basement membrane disease (TBMD) occurs in 5–11% of renal biopsy series, and can be associated with other glomerulopathies (GNs). Data on the prevalence, clinical features, and prognosis of TBMD with other GNs are limited.

Arterial stiffness correlated with cardiac remodelling in patients with chronic kidney disease

Background:  It is well known that both pressure and volume overloads contribute to left ventricular hypertrophy (LVH) and left ventricular dilatation in patients with chronic kidney disease (CKD). Few studies have evaluated the association between increased pulse wave velocity (PWV) and LVH in CKD patients not yet receiving dialysis. The purpose of this study was to assess the relationship between arterial stiffness and cardiac remodelling in patients with CKD, and to determine the independent factors associated with increased left ventricular mass index (LVMI) and left ventricular volume index (LVVI).

Systemic lupus erythematosus presented as non-inflammatory necrotizing vasculopathy-induced ischemic glomerulopathy and small vessels-related ischemic cardiomyopathy

The clinical significance of lupus non-inflammatory necrotizing vasculopathy (NINV) is not well established. For example, since lupus renal NINV is usually reported to coexist with proliferative and active glomerulonephritis, it is difficult to demonstrate the role of NINV on renal pathophysiology. Here we report a 16-year-old SLE boy with renal NINV presenting as ischemic glomerulopathy and small vessels-related ischemic heart failure. The renal biopsy demonstrated mild proliferative glomerulonephritis and NINV initially, and one month later repeated renal biopsy showed NINV with ischemic glomerulopathy. These findings established that NINV, but not proliferative glomerulonephritis, was responsive for his acute renal failure (ARF). Another interesting question is about the pathophysiology of his myocardial dysfunction. This patient presented typical angina and congestive heart failure (CHF). Echocardiograms and ventriculography revealed dilatation of four chambers and low ejection fraction. Serial electrocardiograms demonstrated evolutionary ischemic changes. Coronary angiography revealed no abnormality of large vessels. These findings suggested small vascular lesions-induced myocardial ischemia was the underlying mechanism of dilated cardiomyopathy. As myocardial biopsy was not done in our case, we could only speculate, but not prove, that the NINV observed in renal biopsy may also involve in cardiac microvascular beds. Nevertheless, this interesting case emphasized the role of obliterative small vascular lesions in the pathophysiologyof ARF and myocardial dysfunction. The patient was treated with high-dose corticosteroid, plasma infusion and hemodialysis. His cardiac function improved gradually, however the renal function did not recover.

Extreme metabolic alkalosis treated with normal bicarbonate hemodialysis

Metabolic alkalosis (MA), defined as a primary increment in plasma bicarbonate concentration, is a common complication in hospitalized patients and is associated with high morbidity and mortality in severe cases. One of the major routes of compensation for MA (ie, the secretion of an alkaline urine) is lost in renal failure patients. We report three cases involving four episodes of extreme MA with an arterial pH value greater than 7.60, serum bicarbonate concentration greater than 55 mmol/L, and stupor or seizure. Profound vomiting or massive gastric drainage combined with concurrent oliguric renal failure was the underlying mechanism for severe MA. Hydration and normal central venous pressure failed to improve the MA. The extreme MA was reversed quickly and safely by conventional hemodialysis with normal bicarbonate dialysate of 25 to 28 mmol/L. To our knowledge, this is the first reported successful use of normal bicarbonate dialysate in the treatment of severe MA. We also found that either H(2) blockers or proton-pump inhibitors have a prophylactic effect on the formation of MA.

Incidence, transmission, and clinical significance of hepatitis G virus infection in hemodialysis patients.

Abstract A high prevalence of hepatitis G virus (HGV) infection has been noted in patients receiving chronic hemodialysis (HD) therapy, yet the incidence rate and transmission route have rarely been reported. Serum samples from 160 chronically uremic patients in a HD unit were initially collected at the time chronic HD therapy was begun, and thereafter annually in July and, finally, in November 1999. Serum HGV RNA was detected using nested reverse transcription polymerase chain reaction, and HGV E2 antibody was determined using an enzyme immunoassay. Nucleotide sequences of the 5′-noncoding region were studied in the HD patients with HGV viremia. Forty healthy staff members were also enrolled as control subjects. Three of the 40 (7.5%) healthy staff members were positive for HGV RNA or HGV E2 antibodies, in contrast to 40 of the 160 (25%) HD patients, including 14 (8.8%) who were positive for HGV RNA only, 25 (15.6%) who were positive for HGV E2 antibody only, and 1 (0.6%) who had both markers. HGV exposure did not correlate with gender, age, duration of HD therapy, or history of blood transfusions. At least 20 of the 40 (50%) patients with HGV exposure had been infected before the start of chronic HD therapy. Nevertheless, at least nine (22.5%) patients acquired new HGV infections after starting chronic HD therapy, with an incidence rate of ≥2.6% per year. Three patients with newly acquired HGV viremia after HD therapy was started and two with pre-existing HGV viremia before HD therapy was started had the same nucleotide sequences. HGV and HCV infections (with a prevalence of 14.4%) might have been transmitted independently in HD patients. In addition, HGV infection was not found to cause significant elevation of alanine aminotransferase levels in the group exposed to HGV. To conclude, the incidence of new HGV infections was at least 2.6% per year. In addition to transmission through blood transfusion, HGV may have been transmitted nosocomially patient-to-patient within the HD unit. The compliance with standard universal precautions should be carefully re-examined, but it is not necessary to routinely screen for HGV infection among patients on chronic HD.

The selection of triple therapy for Helicobacter pylori eradication in chronic renal insufficiency

Aim: To establish a triple therapy regimen for Helicobacter pylori eradication in patients with chronic renal insufficiency.

Clinical characteristics and outcomes of new uremic patients with extreme azotemia in southern Taiwan

Serum creatinine (SCr) had been considered to be an important predictor of mortality in end‐stage renal disease (ESRD) patients at the start of renal replacement therapy (RRT). However, the data were limited about initially extreme azotemia (EA), exclusively defined as blood urea nitrogen (BUN)≥300 mg/dL, SCr≥30 mg/dL, or both. This retrospective study was conducted to clarify the characteristics and outcome in our EA patients. We had 1682 new ESRD patients from July 1988 to December 1996. With frequency match for age, gender, and starting RRT in the same period, 20 EA patients and 60 controls were included. Fifty percent of our EA patients had unknown etiology. The EA patients had significantly lower prevalence of underlying diabetic nephropathy, and comorbid hypertension. All the EA patients had late referral to nephrologists within 4 weeks before the initiation of RRT, and 90% of them had taken Chinese herbals. The EA group had significantly higher BUN, SCr, and iron storage as well as a higher prevalence of severe anemia, hyperkalemia, hypocalcemia, and acidemia. However, the similar prevalence of cardiomegaly and left ventricular hypertrophy as well as the similar early mortality rate and long‐term survival were noted. Age over 40 years, comorbid diabetes mellitus, and hypoalbuminemia were independent predictors of poor survival. Our EA patients had different initial presentations from other uremic ones at the start of RRT. However, the short‐term and long‐term mortality rates were similar. The lower prevalence of underlying diabetic nephropathy and comorbid hypertension among the EA patients might contribute to their fair outcome.

Diffuse Calcinosis and Intradermal Tophi in a Uremic Patient: Effect of Low-Calcium Hemodialysis and Mechanism of Hypercalcemia

Soft tissue calcification is a frequent complication in end-stage renal disease (ESRD) patients with a high serum calcium-phosphate product, but systemic involvement of both the visceral organs and skin is rarely seen. We report on a newly diagnosed ESRD patient with gouty nephropathy who had initial presentations of extensive intradermal tophi, diffuse calcinosis, and hypercalcemia. He received maintenance hemodialysis (HD) with low-calcium dialysate (1.25 mEq/l) for 11 months. Although the above complications diminished, serum calcium remained elevated. Thereafter, unexpected cervical lymphadenitis from a Mycobacterium tuberculosis (TB) infection with high extra-renal production of calcitriol was found. Serum calcium levels normalized only after anti-TB treatment for 2 months. We thought that this patient might have had occult TB infection before the start of HD, which resulted in calcitriol production and hypercalcemia. In addition, concomitant hyperphosphatemia in chronic renal failure contributed to severe diffuse calcinosis. After the initiation of HD therapy, both the elevated serum calcitriol levels and accelerated resolution and mobilization of diffuse calcinosis from low-calcium HD contributed to persistent hypercalcemia.

Portal Vein Gas in a Diabetic Patient with Gas-forming Pararenal Abscess

The incidence of portal vein gas (PVG), which used to be an ominous sign of intestinal sepsis, has increased with progressive improvements in imaging modalities. Therefore, the clinical significance of PVG has changed. Emphysematous pyelonephritis (EPN) is a rare, potentially life-threatening and gas-forming infection of the renal parenchyma and/or its surroundings. Gas-forming pararenal abscess presenting with PVG is even rarer. We hereby present the case of a diabetic female with poor glycemic control, who was diagnosed to have EPN and PVG concurrently by computed tomography. She underwent percutaneous catheter drainage (PCD) of the pyelonephritis. Both cultures of blood and pus grew Klebsiella pneumoniae. Her subsequent clinical course was uneventful. In summary, EPN is a rare but potentially fatal urinary tract infection in diabetic patients, and finding PVG on computed tomography can aid in diagnosis. Conservative treatment with intravenous antibiotics and PCD of pus may be adequate for the patient with EPN. However, nephrectomy may be necessary if the patient deteriorates and PCD fails to contain the infection.