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Time-restricted feeding (TRF), devoid of calorie restriction, is acknowledged for promoting metabolic health and mitigating various chronic metabolic diseases. While TRF exhibits widespread benefits across multiple tissues, there is limited exploration into its impact on kidney function. In this study, our aim was to investigate the potential ameliorative effects of TRF on kidney damage in a mouse model of cisplatin-induced acute kidney injury (AKI). Methods: Cisplatin-induced AKI was induced through intraperitoneal injection of cisplatin into C57BL/6 male mice. Mice undergoing TRF were provided unrestricted access to standard chow daily but were confined to an 8-hour feeding window during the dark cycle for 2 weeks before cisplatin injection. The mice were categorized into four groups: control, TRF, cisplatin, and TRF + cisplatin. Results: The tubular damage score and serum creatinine levels were significantly lower in the TRF + cisplatin group compared to the cisplatin group. The TRF + cisplatin group exhibited reduced expression of phosphorylated nuclear factor kappa B, inflammatory cytokines, and F4/80-positive macrophages compared to the cisplatin group. Furthermore, oxidative stress markers for DNA, protein, and lipid were markedly decreased in the TRF + cisplatin group compared to the cisplatin group. TUNEL-positive tubular cells, cleaved caspase-3 expression, and the Bax/Bcl-2 ratio in the TRF + cisplatin group were lower than those in the cisplatin group. Conclusion: TRF, without calorie restriction, effectively mitigated kidney damage by suppressing inflammatory reactions, oxidative stress, and tubular apoptosis in a mouse model of cisplatin-induced AKI. TRF holds promise as a novel dietary intervention for preventing cisplatin-induced AKI.
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Background/Aims@#Acute kidney injury (AKI) is an underestimated yet important risk factor for the development of chronic kidney disease (CKD), characterized by tubulointerstitial fibrosis and tubular dedifferentiation. Tubular dedifferentiation, which is associated with the loss of epithelial markers and the gain of mesenchymal features, is thought to be involved in tubulointerstitial fibrosis. As protein kinase B/Akt is involved in the development of CKD, we investigated the role of Akt1, one of the three Akt isoforms, in a murine model of AKI-to-CKD progression. @*Methods@#We subjected C57BL/6 male mice to unilateral ischemia-reperfusion injury (UIRI) and harvested their kidneys after 6 weeks. Mice were divided into four groups, namely, wild-type (WT) UIRI, Akt1−/− UIRI, WT sham, and Akt1−/− sham. @*Results@#Akt1 (but not Akt2 or Akt3) was markedly activated in WT UIRI mice than in WT sham mice. Tubulointerstitial fibrosis and tubular dedifferentiation significantly increased in WT UIRI mice, but were attenuated in Akt1−/− UIRI mice. Both WT UIRI and Akt1−/− UIRI mice showed markedly upregulated transforming growth factor-β1 (TGF-β1)/Smad signaling compared with WT sham mice. However, TGF-β1/Smad expression did not differ between the two groups. The levels of phosphorylated GSK-3β, β-catenin, and Snail were attenuated in Akt1−/− UIRI mice compared with those in WT UIRI mice. @*Conclusions@#Deletion of Akt1 results in the attenuation of renal fibrosis and tubular dedifferentiation, independent of TGF-β1/Smad signaling, during AKI-to-CKD progression in a UIRI without contralateral nephrectomy model. Thus, Akt1 may serve as a therapeutic target in AKI-to-CKD progression.
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Background@#Data on liver cirrhosis (LC) patients undergoing continuous renal replacement therapy (CRRT) are lacking despite the dismal prognosis. We therefore evaluated clinical characteristics and predictive factors related to mortality in LC patients undergoing CRRT. @*Methods@#We performed a retrospective observational study at two tertiary hospitals in Korea. A total of 229 LC patients who underwent CRRT were analyzed. Patients were classified into survivor and non-survivor groups. We used multivariable Cox regression analyses to identify factors predictive of in-hospital mortality. @*Results@#During a median follow-up of 5 days (interquartile range, 1–19 days), in-hospital mortality rate was 66.4%. In multivariable analysis, the Acute Physiology and Chronic Health Evaluation II (APACHE II) score (hazard ratio [HR], 1.03; 95% confidence interval [CI], 1.01–1.06; p = 0.02), Model for End-Stage Liver Disease (MELD) score (HR, 1.08; 95% CI, 1.04–1.11; p 35 mL/kg/hr (HR, 3.13; 95% CI, 1.62–6.05; p = 0.001). Subgroup analysis revealed that a CRRT delivered dose < 25 mL/kg/hr was a significant risk factor for in-hospital mortality among LC patients with a MELD score ≥ 30. @*Conclusion@#High APACHE II score, high MELD score, and low delivered CRRT dose were significant risk factors for in-hospital mortality. CRRT delivered dose impacted mortality significantly, especially in patients with a MELD score ≥ 30.
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Background/Aims@#Acute kidney injury (AKI) is an underestimated yet important risk factor for the development of chronic kidney disease (CKD), characterized by tubulointerstitial fibrosis and tubular dedifferentiation. Tubular dedifferentiation, which is associated with the loss of epithelial markers and the gain of mesenchymal features, is thought to be involved in tubulointerstitial fibrosis. As protein kinase B/Akt is involved in the development of CKD, we investigated the role of Akt1, one of the three Akt isoforms, in a murine model of AKI-to-CKD progression. @*Methods@#We subjected C57BL/6 male mice to unilateral ischemia-reperfusion injury (UIRI) and harvested their kidneys after 6 weeks. Mice were divided into four groups, namely, wild-type (WT) UIRI, Akt1−/− UIRI, WT sham, and Akt1−/− sham. @*Results@#Akt1 (but not Akt2 or Akt3) was markedly activated in WT UIRI mice than in WT sham mice. Tubulointerstitial fibrosis and tubular dedifferentiation significantly increased in WT UIRI mice, but were attenuated in Akt1−/− UIRI mice. Both WT UIRI and Akt1−/− UIRI mice showed markedly upregulated transforming growth factor-β1 (TGF-β1)/Smad signaling compared with WT sham mice. However, TGF-β1/Smad expression did not differ between the two groups. The levels of phosphorylated GSK-3β, β-catenin, and Snail were attenuated in Akt1−/− UIRI mice compared with those in WT UIRI mice. @*Conclusions@#Deletion of Akt1 results in the attenuation of renal fibrosis and tubular dedifferentiation, independent of TGF-β1/Smad signaling, during AKI-to-CKD progression in a UIRI without contralateral nephrectomy model. Thus, Akt1 may serve as a therapeutic target in AKI-to-CKD progression.
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Background@#Urgent-start peritoneal dialysis (PD) is applied to patients who need PD within two weeks but are able to wait for more than 48 hours before starting PD. To evaluate the usefulness of percutaneous PD catheter insertion in urgent-start PD, we reviewed the clinical outcomes of percutaneous catheter insertion with immediate start PD and surgical insertion with longer break-in time in Pusan National University Hospital. @*Methods@#This study included 177 patients who underwent urgent-start PD. Based on the PD catheter insertion techniques, the patients with urgent-start PD were divided into percutaneous (n = 103) and surgical (n = 74) groups. For the percutaneous group, a modified Seldinger percutaneous catheter insertion with immediate initiation of continuous ambulatory PD was performed by nephrologists. @*Results@#The percutaneous group showed higher serum urea nitrogen, creatinine, and lower serum albumin compared with the surgical group (P < 0.05). Ninety-day infectious and mechanical complications showed no significant differences between the two groups. Ninety-day peritonitis in the percutaneous group was 9.7% compared to 5.4% in the surgical group (P = not significant [NS]). Major leakage was 3.9% in the percutaneous group compared to 1.4% in the surgical group (P = NS). Overall infectious and mechanical complication-free survival was not significantly different between the two groups. The percutaneous group and surgical group showed no statistical difference with respect to catheter survival over the entire observation period (P = NS). @*Conclusion@#This study suggests that urgent-start PD can be applied safely with percutaneous catheter insertion by nephrologists with no break-in period.
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BACKGROUND: This study was undertaken to explore the effects of aging on the kidneys in mouse models of diabetes and chronic kidney disease (CKD), and to compare the expression of two isoforms of matrix metalloproteinase-2 (MMP-2)–secretory full-length MMP-2 and intracellular N-terminal truncated MMP-2 (NTT-MMP-2)–in these models. METHODS: Two experimental ICR mouse models were used: a streptozotocin (STZ)-induced type 1 diabetes mellitus model and a 5/6 nephrectomized (5/6Nx) CKD model. The abundance of each isoform of MMP-2 was determined by quantitative polymerase chain reaction (qPCR), and functional analyses were conducted. Moreover, the protein levels of the two MMP-2 isoforms were determined semi-quantitatively by immunohistochemical staining, and their association with tissue damage was assessed. RESULTS: Both isoforms of MMP-2 were upregulated in the kidney tissues of STZ-induced diabetic mice and 5/6Nx mice, irrespective of age. Characteristically, NTT-MMP-2 protein expression was elevated in old control mice, in line with the qPCR results. NTT-MMP-2 expression was limited to the renal cortex, and to the tubulointerstitial area rather than the glomerular area. In terms of tissue damage, tubulointerstitial fibrosis was more severe in old 5/6Nx mice than in their young counterparts, whereas glomerulosclerosis was comparable in old and young 5/6Nx mice. CONCLUSION: The intracellular isoform of MMP-2 was induced by ageing, irrespective of the presence of diabetes or CKD, and its induction may be related to tubulointerstitial fibrosis in chronic kidney disease.
Subject(s)
Animals , Mice , Aging , Diabetes Mellitus , Diabetes Mellitus, Type 1 , Fibrosis , Kidney , Matrix Metalloproteinase 2 , Mice, Inbred ICR , Polymerase Chain Reaction , Protein Isoforms , Renal Insufficiency, Chronic , StreptozocinABSTRACT
This report describes a case of severe hypernatremia with a serum sodium concentration of 188.1mmol/L caused by exogenous salt intake. A 26-year-old man diagnosed with Crohn's disease 5 years previously visited our clinic due to generalized edema and personality changes, with aggressive behavior. He had compulsively consumed salts, ingesting approximately 154 g of salt over the last 4 days. Despite careful fluid management that included not only hypotonic fluid therapy for 8 hours but also hypertonic saline administration, his serum sodium level decreased sharply at 40.6 mmol/L; however, it returned to normal within 72-hour of treatment without any neurological deficits. Primary hypothyroidism was also diagnosed. He was discharged after 9 days from admission, with a stable serum sodium level. We have described the possibility of successful treatment in a patient with hypernatremia caused by acute salt intoxication without sustained hypotonic fluid therapy.
Subject(s)
Adult , Humans , Crohn Disease , Edema , Fluid Therapy , Hypernatremia , Hypothyroidism , Salts , SodiumABSTRACT
We report 2 cases of chronic estimated glomerular filtration rate (eGFR) decline after unilateral adrenalectomy due to primary aldosteronism. The patients were diagnosed with unilateral adrenal cortical adenoma releasing aldosterone. Two patients were examined for hypertension and hypokalemia. Unilateral laparoscopic adrenalectomy was performed in both cases, and pathology confirmed adrenal cortical adenoma. After adrenalectomy, hypertension and hypokalemia improved to within normal range. However, the eGFR decreased postoperatively, and abdominal computed tomography scan showed decreased kidney size compared to previous images. Kidney biopsy was performed to delineate the exact cause of renal function deterioration and revealed hypertensive changes with chronic interstitial changes, indicating that glomerular hyperfiltration with aldosterone excess masked renal function damage. Physicians have to consider the probability of postadrenalectomy eGFR decline related to chronic hypertensive change.
Subject(s)
Humans , Adrenalectomy , Adrenocortical Adenoma , Aldosterone , Biopsy , Glomerular Filtration Rate , Hyperaldosteronism , Hypertension , Hypokalemia , Kidney , Masks , Pathology , Reference Values , Renal Insufficiency, ChronicABSTRACT
BACKGROUND/AIMS: Tubulointerstitial injury plays an important role in the progression of immunoglobulin A nephropathy (IgAN), and neutrophil gelatinase-associated lipocalin (NGAL) is among the most sensitive tubular biomarkers. We investigated whether serum or urine NGAL predicts prognosis in patients with IgAN. METHODS: The present study enrolled patients with biopsy-proven IgAN from January 2005 to December 2010, whose serum and urine samples at the time of kidney biopsy were preserved by freezing. We retrospectively reviewed patient clinical data and followed patients until October 2012. Serum and urine NGAL levels were measured using an enzyme-linked immunosorbent assay kit. Renal progression was defined as an estimated glomerular filtration rate decline by > 50% or progression to end-stage renal disease. RESULTS: There were 121 patients enrolled in this study. During the median follow-up period of 41.49 months, renal progression was found in nine patients (7.4%). Serum or urine NGAL alone could not predict renal progression; however, when serum and urine NGAL levels were combined, belonging to the high NGAL group independently predicted renal progression (hazard ratio [HR], 5.56; 95% confidence interval [CI], 1.42 to 21.73; p = 0.014), along with tubular damage graded according to the Oxford classification as T2 (HR, 8.79; 95% CI, 2.01 to 38.51; p = 0.004). In addition, a Kaplan-Meier curve of renal survival showed significantly higher renal progression in patients in the high NGAL group (log rank, p = 0.004). CONCLUSIONS: In patients with IgAN, high serum and urine NGAL levels at the time of kidney biopsy predict renal progression.
Subject(s)
Adult , Female , Humans , Male , Middle Aged , Young Adult , Acute-Phase Proteins/urine , Biomarkers/blood , Biopsy , Chi-Square Distribution , Disease Progression , Enzyme-Linked Immunosorbent Assay , Glomerular Filtration Rate , Glomerulonephritis, IGA/blood , Kaplan-Meier Estimate , Kidney/metabolism , Lipocalins/blood , Multivariate Analysis , Predictive Value of Tests , Prognosis , Proportional Hazards Models , Proto-Oncogene Proteins/blood , Retrospective Studies , Risk FactorsABSTRACT
A 74-yr-old woman presented with fever and abdominal discomfort. She was in a septic condition caused by urinary tract infection. Her computed tomogram of the abdomen revealed features of hydronephrosis with ureteral stones in both kidneys. During percutaneous nephrostomies, right pyeloduodenal fistula (PDF) was diagnosed. Elective surgery was originally planned but the patient was in a poor condition to undergo surgery. Instead, 2 times endoscopic clipping and ligation by endoloop were applied with parenteral antibiotics for the fistula lesion. On admission day 30, she was discharged from the hospital after confirmation of no more contrast leakage on fistulography. We reviewed the literature and discuss the etiologies, clinical presentations, diagnosis, and treatment of PDF.
Subject(s)
Aged , Female , Humans , Duodenal Diseases/complications , Hydronephrosis/complications , Intestinal Fistula/complications , Kidney/diagnostic imaging , Kidney Calculi/complications , Kidney Diseases/complications , Ligation , Urethral Obstruction/complications , Urinary Fistula/complications , Urinary Tract Infections/complicationsABSTRACT
BACKGROUND: We aimed to evaluate the performance of serum cystatin C-based equations in calculating the glomerular filtration rate (GFR) in patients with varying stages of chronic kidney disease (CKD). METHODS: Serum cystatin C and creatinine levels were measured in 615 CKD patients. The CKD stage was determined by the creatinine-based estimated GFR (eGFR) equation using the four-variable abbreviated Modification of Diet in Renal Disease equation suggested by the Kidney Disease Outcome Quality Initiative with the addition of a coefficient applicable to Korean populations (K-aMDRD). In each CKD stage, the ratio of serum cystatin C to creatinine was calculated and six different cystatin C-based equations were used to estimate GFR. Cystatin C-based eGFR and aMDRD eGFR values were compared using the paired t test, Pearson correlation test, and the Bland-Altman plot. RESULTS: The mean age of patients was 53.21+/-14.45 years; of the 615 patients, 346 were male. The serum cystatin C-to-creatinine ratio was inversely correlated with the CKD stage. Compared with the K-aMDRD values, the results of the Hoek, Filler, and Le Bricon's cystatin C-based eGFR equations were lower in CKD Stages 1-3 and higher in Stages 4 and 5. However, the results of the Orebro-cystatin (Gentian) equation [GFR=100/ScytC (mL/minute/1.73m2) - 14] were similar to those of the K-aMDRD equation in CKD Stages 4 and 5 (15.44+/-9.45 vs. 15.17+/-9.05mL/minute/1.73m2, respectively; P=0.722; bias=0.27+/-8.87). CONCLUSION: The eGFRs obtained from the six cystatin C-based equations differed widely. Therefore, further studies are required to determine the most accurate equation to estimate GFR in Koreans with CKD.
Subject(s)
Humans , Male , Creatinine , Cystatin C , Diet , Glomerular Filtration Rate , Kidney Diseases , Renal Insufficiency, ChronicABSTRACT
The authors regret that, in the above article, one of the co-authors' names was incorrectly printed. It is now reproduced correctly above.
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Coronary artery disease (CAD) is the leading cause of death in patients with chronic kidney disease (CKD).Although many studies have shown a higher prevalence of CAD among these patients, the association between the spectrum of renal dysfunction and severity of CAD remains unclear. In this study, we investigate the association between renal function and the severity of CAD. We retrospectively reviewed the medical records of 1,192 patients who underwent elective coronary angiography (CAG). The severity of CAD was evaluated by Gensini score according to the degree of luminal narrowing and location(s) of obstruction in the involved main coronary artery. In all patients, the estimated glomerular filtration rate (eGFR) was independently associated with Gensini score (beta=-0.27, P < 0.001) in addition to diabetes mellitus (beta=0.07, P = 0.02), hypertension (beta=0.12, P < 0.001), low density lipoprotein (LDL)-cholesterol (beta=0.08, P = 0.003), and hemoglobin (beta=-0.07, P = 0.03) after controlling for other confounding factors. The result of this study demonstrates that decreased renal function is associated not only with the prevalence, but also the severity, of CAD.
Subject(s)
Female , Humans , Male , Middle Aged , Cholesterol, LDL/blood , Coronary Angiography , Coronary Artery Disease/complications , Diabetes Mellitus , Glomerular Filtration Rate , Hemoglobins/metabolism , Hypertension/complications , Kidney , Kidney Function Tests , Organ Dysfunction Scores , Renal Insufficiency, Chronic/complications , Retrospective Studies , Severity of Illness IndexABSTRACT
A 56-year-old male with pulmonary tuberculosis was admitted to our hospital for evaluation of generalized edema. He began antituberculosis treatment with rifampin, isoniazid, ethambutol, and pyrazinamide. He experienced abnormal increments in weight and serum creatinine after 6 weeks. All serological findings, including anti-neutrophil cytoplasmic antibodies (ANCA), were negative. Rifampin was stopped because it might have caused the increase in creatinine. Renal biopsy was consistent with pauci-immune crescentic glomerulonephritis (CrGN). His renal function was improved by high-dose steroid treatment. Rifampin-induced, ANCA-negative pauci-immune CrGN is very rare; most cases of rifampin-induced acute renal failure are due to acute tubulointerstitial nephritis. We present here a case of rifampin-induced CrGN and pulmonary tuberculosis successfully treated with high-dose steroids and antituberculosis medications, excluding rifampin.
Subject(s)
Humans , Male , Middle Aged , Acute Kidney Injury , Antibodies, Antineutrophil Cytoplasmic , Biopsy , Creatinine , Edema , Ethambutol , Glomerulonephritis , Isoniazid , Nephritis, Interstitial , Pyrazinamide , Rifampin , Steroids , Tuberculosis, PulmonaryABSTRACT
BACKGROUND/AIMS: Accumulating data suggest that vitamin D deficiency is prevalent in patients with chronic kidney disease (CKD). However, comprehensive data are lacking for Koreans. The aim of this study was to survey vitamin D deficiency among patients with CKD in Korea and to identify the relationships among various factors. METHODS: We conducted a retrospective cohort study of 444 patients who were divided into four subgroups by estimated glomerular filtration rate (eGFR) for comparisons of mean 25-hydroxyvitamin D [25(OH)D] level and other parameters. In addition, non-dialyzed patients were categorized into four groups based on 25(OH)D levels ( or =30 ng/mL), and risk factors for severe vitamin D deficiency ( or = 60 mL/min/1.73 m2, 43% (34/79) showed severe 25(OH)D deficiency, and the mean 25(OH)D level was 11.7 +/- 5.3 ng/mL. In CKD3 group, 53.2% (41/77) showed severe 25(OH)D deficiency, with a mean level of 11.3 +/- 7.2 ng/mL. In CKD4 group, 53.3% (49/92) had severe 25(OH)D deficiency, with a mean level of 11.0 +/- 6.2 ng/mL. Approximately 71% (139/196) of patients in CKD5 group showed severe deficiency, and the mean level was 9.2 +/- 5.9 ng/mL. Severe 25(OH)D deficiency was affected by winter season, renal function, diabetes, and low-density lipoprotein cholesterol. The serum parathyroid hormone level was inversely correlated with the 25(OH)D level, such that 25(OH)D <20 ng/mL were associated with a steep increase in parathyroid hormone. CONCLUSIONS: Vitamin D deficiency is highly prevalent in the Korean population. Few patients met a sufficient 25(OH)D concentration, even in the early stages of CKD. Our data suggest that 25(OH)D level of 20 ng/mL is a threshold for a rapid increase in parathyroid hormone levels.
Subject(s)
Humans , Cholesterol , Cohort Studies , Glomerular Filtration Rate , Korea , Lipoproteins , Parathyroid Hormone , Renal Insufficiency, Chronic , Retrospective Studies , Risk Factors , Seasons , Vitamin D , Vitamin D DeficiencyABSTRACT
BACKGROUND: Despite using renin-angiotensin system (RAS) blockades, some of the patients with immunoglobulin A (IgA) nephropathy often had persistent proteinuria of more than 500mg/d. They need to be managed further by alternative methods to halt the progression of the disease; these methods could also be applied safely over a long period of time. In this context, sulodexide has been studied for the management of diabetic nephropathy. METHODS: A retrospective review was carried out involving 20 patients with IgA nephropathy who had been taking sulodexide (50mg daily) as an add-on therapy together with an optimal dose of RAS blockades during 2008-2009. We evaluated the proteinuria reduction rates and renal function changes. RESULTS: During 11.1+/-72.7 months of follow-up duration, urinary protein-to-creatinine ratio (UPCR) decreased for 1.57+/-0.6 to 1.17+/-0.7 g/g (P=0.032). Twenty-five percent of the patients showed a greater than 50% reduction of UPCR, and 40% had a UPCR of less than 1.0g/g at their final observations. The analysis of the factors contributing to the effect found that a higher pretreatment UPCR showed a significant correlation with the UPCR decrease (r=0.45, P=0.047). Neither the adverse effects nor the renal function impairments were documented during the management. CONCLUSION: Low-dose sulodexide has an additional modest antiproteinuric effect on IgA nephropathy undergoing RAS blockade therapy.
Subject(s)
Humans , Follow-Up Studies , Glomerulonephritis, IGA , Glycosaminoglycans , Immunoglobulin A , Proteinuria , Renin-Angiotensin System , Retrospective StudiesABSTRACT
BACKGROUND/AIMS: Cardiovascular complications are commonly seen in patients with chronic kidney disease (CKD). Recently, the prevalence of left ventricular diastolic dysfunction (LVDD) has increased, and the importance of LVDD has emerged in patients with CKD. The objectives of this study were to identify diagnostic criteria for LVDD related to ischemic heart disease (IHD) and evaluate the prognostic impact of diastolic dysfunction in patients with CKD. METHODS: A total of 71 patients with CKD who were evaluated between January 2005 and May 2010 were included in this study. These patients were evaluated by conventional echocardiography and tissue Doppler imaging (TDI) for diastolic dysfunction. RESULTS: Diagnostic cutoff values for LVDD related to IHD were E/E' = 15.55 (sensitivity: 100%, specificity: 64.7%, p = 0.005) and E/A = 0.79 (sensitivity: 84.6%, specificity: 55.9%, p = 0.006). Group I consisted of 19 patients with an E/E' > 15.55 and E/A > 0.79. Group II consisted of the remaining patients. Factors contributing to LVDD were age, history of ischemic heart disease, anemia, and high low-density lipoprotein (LDL) level. Factors contributing to IHD were LVDD, smoking, high LDL level, and high parathyroid hormone (PTH) level. The disease-free survival for IHD was significantly lower in group I compared to group II (p = 0.001). However, there was no significant difference in overall survival between groups I and II (p = 0.177). CONCLUSIONS: Our study showed that moderate LVDD (E/E' > 15.55 and E/A > 0.79) in patients with CKD is positively associated with IHD.
Subject(s)
Humans , Anemia , Disease-Free Survival , Echocardiography , Heart Failure, Diastolic , Lipoproteins , Myocardial Ischemia , Parathyroid Hormone , Prevalence , Renal Insufficiency , Renal Insufficiency, Chronic , Smoke , SmokingABSTRACT
BACKGROUND/AIMS: Because preoperative diagnosis of xanthogranulomatous pyelonephritis (XGP) is difficult, due to its similarities to other renal diseases, the diagnosis is made postoperatively in most cases. The purpose of this study was to describe the clinical findings in 11 patients with histologically documented XGP. METHODS: We retrospectively reviewed the characteristics, laboratory and radiological findings, preoperative diagnoses and operative methods of 11 patients with XGP, who underwent a surgical procedure or percutaneous renal biopsy. RESULTS: Among eleven patients, nine had flank pain and six had anemia. Preoperatively, three patients were diagnosed as XGP, two with renal cell carcinoma, two with renal tuberculosis, one with renal abscess, one with perirenal abscess, one with renal staghorn calculi with non-functioning kidney, and one with pyelonephrosis. On the basis of the computed tomography (CT) features, the diffuse or global forms (70.0%) were more common than the localized or focal forms (30.0%). One patient diagnosed with renal cell carcinoma preoperatively was diagnosed as XGP through an intraoperative frozen section renal tissue biopsy and underwent partial nephrectomy. One patient diagnosed as focal XGP underwent percutaneous biopsy of the renal mass, which confirmed the diagnosis. This patient received treatment with only antibiotic therapy. CONCLUSIONS: CT can be considered the preferred diagnostic tool for the evaluation of XGP; however, percutaneous renal biopsy seems to be valuable in selected cases for differential diagnosis of renal malignancy.
Subject(s)
Humans , Abscess , Anemia , Anti-Bacterial Agents , Biopsy , Calculi , Carcinoma, Renal Cell , Diagnosis, Differential , Flank Pain , Frozen Sections , Kidney , Nephrectomy , Pyelonephritis, Xanthogranulomatous , Retrospective Studies , Tuberculosis, RenalABSTRACT
A 56-year-old male with pulmonary tuberculosis was admitted to our hospital for evaluation of generalized edema. He began antituberculosis treatment with rifampin, isoniazid, ethambutol, and pyrazinamide. He experienced abnormal increments in weight and serum creatinine after 6 weeks. All serological findings, including anti-neutrophil cytoplasmic antibodies (ANCA), were negative. Rifampin was stopped because it might have caused the increase in creatinine. Renal biopsy was consistent with pauci-immune crescentic glomerulonephritis (CrGN). His renal function was improved by high-dose steroid treatment. Rifampin-induced, ANCA-negative pauci-immune CrGN is very rare; most cases of rifampin-induced acute renal failure are due to acute tubulointerstitial nephritis. We present here a case of rifampin-induced CrGN and pulmonary tuberculosis successfully treated with high-dose steroids and antituberculosis medications, excluding rifampin.