Serum Uric Acid and Risk for Acute Kidney Injury Following Contrast.

Contrast-induced acute kidney injury (CI-AKI) is a common cause of hospital-acquired acute kidney injury (AKI). We evaluated the evidence that uric acid (UA) plays a pathogenic role in CI-AKI. Ten studies were eligible for inclusion for meta-analysis. Hyperuricemia predicted risk for cases with AKI in prospective cohort studies. Higher levels of serum UA (SUA), as defined by the authors, were associated with a 2-fold increased risk to develop AKI (pooled odds ratio 2.03; 95% confidence interval [CI] 1.48-2.78). Significant heterogeneity was found in cohort studies ( P = .001, I2 = 85.7%). In 2 clinical trials, lowering of SUA with saline hydration was significantly associated with reduced risk for AKI compared with saline hydration alone or saline hydration with N-acetyl cysteine. An analysis of 2 randomized controlled trials found that allopurinol with saline hydration had a significant protective effect on renal function (assessed by serum creatinine values) compared with hydration alone (mean difference: -0.52 mg/dL; 95% CI: -0.81 to -0.22). Hyperuricemia independently predicts CI-AKI. Two clinical trials suggest lowering SUA may prevent CI-AKI. The mechanism by which UA induces CI-AKI is likely related to acute uricosuria.

Colchicine in Renal Medicine: New Virtues of an Ancient Friend.

Colchicine is a plant-derived alkaloid that disrupts the cell microtubule system and accumulates in neutrophils, inhibiting neutrophil adhesion and recruitment. Colchicine has been used extensively in the prevention and treatment of gouty arthritis attacks, familial Mediterranean fever attacks and resultant AA amyloidosis, and recurrent pericarditis. Colchicine also disrupts the intracellular traffic of additional inflammatory and fibrosis mediators. Renal fibrosis is the final common pathway of chronic renal disease. Colchicine had anti-fibrotic effects in experimental diabetic nephropathy, renal mass reduction, and cyclosporine nephrotoxicity among others and is undergoing clinical trials for non-diabetic metabolic syndrome and diabetic nephropathy. In this review, we summarize the anti-inflammatory and anti-fibrotic properties of colchicine in experimental and clinical studies in renal diseases or other fibrotic disease processes with renal consequences. We also discuss the potential future uses of colchicine in renal medicine and challenges faced with its use in patients with impaired kidney function.

Novel Faces of Fibroblast Growth Factor 23 (FGF23): Iron Deficiency, Inflammation, Insulin Resistance, Left Ventricular Hypertrophy, Proteinuria and Acute Kidney Injury.

FGF23 is a hormone that appears as the core regulator of phosphate metabolism. Great deal of data has accumulated to demonstrate increased FGF23 secretion from the bone to compensate for even subtle increases in serum phosphorus long before intact PTH. However, recent evidence points to the fact that actions and interactions of FGF23 are not limited solely to phosphate metabolism. FGF23 may be implicated in iron metabolism and erythropoiesis, inflammation, insulin resistance, proteinuria, acute kidney injury and left ventricular hypertrophy. In this review, we will summarize latest experimental and clinical data examining impact of FGF23 on aforementioned pathophysiologic pathways/disorders.

The role of sodium intake in nephrolithiasis: epidemiology, pathogenesis, and future directions.

The prevalence of nephrolithiasis has doubled over the last decade and the incidence in females now approaches that of males. Since dietary salt is lithogenic, a purported mechanism common to both genders is excess dietary sodium intake vis-a-vis processed and fast foods. Nephrolithiasis has far-reaching societal implications such as impact on gross domestic product due to days lost from work (stone disease commonly affects working adults), population-wide carcinogenic diagnostic and interventional radiation exposure (kidney stone disease is typically imaged with computed tomographic imaging and treated under imaging guidance and follow-up), and rising healthcare costs (surgical treatment will be indicated for a number of these patients). Therefore, primary prevention of kidney stone disease via dietary intervention is a low-cost public health initiative with massive societal implications. This primer aims to establish baseline epidemiologic and pathophysiologic principles to guide clinicians in sodium-directed primary prevention of kidney stone disease.

Novel Masters of Erythropoiesis: Hypoxia Inducible Factors and Recent Advances in Anemia of Renal Disease.

Anemia seen in patients with chronic kidney disease is a particular form of 'anemia of chronic disease'. Although multifactorial in origin, erythropoiesis-stimulating agents (ESAs) and adjuvant iron therapy represent the primary treatment for anemia in chronic kidney disease. Subsequent clinical observations revealed that these ESA hyporesponsive patients often had increased systemic inflammation as a consequence of their comorbidities. Use of high ESA doses to overcome this ESA hyporesponsiveness posed some concerns regarding associated adverse events of therapy and increased mortality in this special patient population. Recognizing the pivotal roles of hypoxia inducible factors (HIFs) in orchestrating elements of erythropoiesis opened new avenues in the management of renal anemia. Several phase 1 and 2 studies confirmed the results of early experimental studies supporting the beneficial role of augmenting HIFs for erythropoiesis. In this review, we describe the physiologic functions of HIF in erythropoiesis with special emphasis on interactions with iron and hepcidin metabolism and inflammation.

Comparison of serum sodium levels measured by blood gas analyzer and biochemistry autoanalyzer in patients with hyponatremia, eunatremia, and hypernatremia.

BACKGROUND: Blood gas analyzer (BGA) electrolyte measurements are frequently used in emergency departments (EDs) pending biochemistry laboratory autoanalyzer (BLA) results. There is lack of data in the literature in terms of agreement of these 2 measurement methods of sodium. We aimed to comprehensively evaluate the agreement in hyponatremia, eunatremia, and hypernatremia groups. METHODS: Retrospectively, adult subjects who presented to ED of a tertiary care teaching hospital and had simultaneous BGA and BLA results were included in the study. Blood pairs were grouped into hyponatremia, eunatremia, and hypernatremia according to BLA results. Agreement of sodium measurements between the methods were evaluated by Bland-Altman plots and Passing and Bablok regression analysis. RESULTS: A total of 2557 blood pairs (1326 males [51.8%]) were included. Median age of the patients was 66 years (18-103). The numbers of patients with hyponatremia, eunatremia, and hypernatremia were 487 (19%), 1943 (76%), and 127 (5%), respectively. The minimum and maximum serum sodium levels measured by biochemistry analyzer were 106 and 171 mmol/L, respectively. The Pearson linear correlation coefficient between BGA and BLA for sodium measurements were 0.574, 0.358, and 0.562 in hyponatremia, eunatremia, and hypernatremia groups, respectively. The absolute mean difference for the 3 groups was greater than 4 mmol/L. Biochemistry laboratory autoanalyzer tended to measure serum sodium higher than BGA in all sodium groups. Passing and Bablok regression analysis showed significant differences between the 2 methods in all sodium groups. CONCLUSION: This is the first comprehensive evaluation of agreement between BGA and BLA in distinct sodium groups. Significant differences should be taken into account when these patients are managed in the ED.

Agreement of serum potassium measured by blood gas and biochemistry analyzer in patients with moderate to severe hyperkalemia.

PURPOSE: Several studies investigated the agreement between central laboratory biochemistry analyzers and blood gas analyzers for potassium measurements. However, data are scarce when the potassium level is moderate to severely high. We aimed to evaluate the agreement between central laboratory biochemistry analyzers and blood gas analyzer in terms of serum potassium level measurement because differences in potassium at this level translate into very different clinical actions. BASIC PROCEDURES: This was a retrospective medical record review study in which patients who presented to the emergency department and had serum potassium levels ≥6mmol/L were included. Patients who did not have simultaneous potassium measurement by blood gas analyzer were excluded. We included all patients meeting potassium criteria irrespective of their underlying disease or comorbidities. We evaluated agreement between the measurement methods with Pearson correlation, Bland-Altman plot, and Sign test. MAIN FINDINGS: A total of 118 blood sample pairs were included. The mean serum potassium level measured by biochemistry analyzer was 6.78±0.79mmol/L, whereas it was 6.16±0.86mmol/L by blood gas analyzer (P<.001, Sign test). There was a strong correlation (P<.001, r=0.864) between the 2 methods, but agreement was relatively poor. Blood gas analyzer tended to measure potassium significantly lower than measured by biochemistry analyzer. The mean difference between the methods was 0.62±0.43mmol/L. PRINCIPAL CONCLUSIONS: In patients with moderate to severe hyperkalemia, blood gas analyzer and biochemistry analyzer gives significantly different serum potassium results which may be clinically important.

Renal artery embolization in severe nephrotic syndrome.

Introduction Severe nephrotic syndrome is associated with increased morbidity and mortality. Renal artery embolization (RAE) has been used in a number of renal diseases such as renal tumors, arteriovenous fistulas etc. However, data regarding benefits of RAE in patients with symptomatic severe proteinuria is limited. We decided to evaluate role of RAE in the setting of severe symptomatic nephrotic syndrome. Methods Eight patients who had undergone transcatheter renal artery embolization with polyvinyl alcohol (PVA) were included. Clinico-demographic characteristics as well as baseline laboratory data including level of proteinuria, serum albumin, C-reactive protein and LDL cholesterol levels were recorded for each patient. After RAE, outpatient clinic control laboratory values were also assessed. Findings All patients except one underwent bilateral RAE (four simultaneous or three sequential). Two patients experienced postembolization syndrome characterized by flank pain, fever, and leukocytosis, which was self-limited and responded to analgesics in all patients. There was no technical complications associated with RAE procedure. All patients became anuric except one. Serum albumin levels increased and serum LDL-cholesterol levels decreased considerably in treated patients. Discussion Renal artery embolization with the purpose of amelioration in nephrotic syndrome complications was effective and free of major technical complications in our patients.

Drug Dose Adjustment in Dialysis Patients Admitted in Clinics Other Than Internal Medicine.

Many drugs that are administered during hospitalization are metabolized or excreted through kidneys, consequently require dosage adjustment. We aimed to investigate inappropriate prescription of drugs requiring renal dose adjustment (RDA) in various surgical and medical inpatient clinics. We retrospectively determined dialysis patients hospitalized between January 2007 and December 2010. Inpatient clinics, including cardiology, pulmonary medicine, neurology, infectious diseases (medical clinics) and cardiovascular surgery, orthopedics, general surgery, obstetrics and gynecology, and neurosurgery (surgical clinics), were screened via electronic database. Total and RDA medications were determined. RDA drugs correctly adjusted to creatinine clearance were labeled as RDA-A (appropriate), otherwise as RDA-I (inappropriate). Renal doses of RDA medications were based on the "American College of Physicians Drug Prescribing in Renal Failure, fifth Edition." Two hundred seventeen hospitalization records of 172 dialysis patients (92 men and 80 women) were included in the analysis. Mean age of patients was 59.4 ± 14.6 years, and the mean hospitalization duration was 8.5 ± 7.8 days. In total, 247 (84.3%, percentage in drugs requiring dose adjustment) and 175 (46.2%) drugs have been inadequately dosed in surgical and medical clinics, respectively. The percentage of patients to whom at least 1 RDA-I drug was ordered was 92% and 91.4% for surgical and medical clinics, respectively (P > 0.05). Nephrology consultation numbers were 8 (7.1%) in surgical and 32 (30.4%) in medical clinics. The most common RDA-I drugs were aspirin and famotidine. A significant portion of RDA drugs was ordered inappropriately both in surgical and medical clinics. Nephrology consultation rate was very low. Measures to increase physician awareness are required to improve results.

Serum neutrophil gelatinase-associated lipocalin is associated with cardiovascular events in patients with chronic kidney disease.

BACKGROUND: Neutrophil gelatinase-associated lipocalin (NGAL) is a member of the lipocalin family best known as a novel and early marker of acute kidney injury (AKI). Recent data suggest that NGQueryAL is not only a marker of AKI, but also an important player in the vascular remodeling, atherosclerotic plaque stability and thrombus formation. We conducted this study to investigate the association of serum NGAL levels with fatal and composite (fatal and non-fatal) cardiovascular events (CVE) in a cohort of patients with stage 1-5 CKD. METHODS: This was an observational cohort study in which serum NGAL was obtained from 298 CKD (stages 1-5) patients. Fatal and composite CVE were recorded for a median 41 months. We examined alteration of serum NGAL through CKD groups as well as association with inflammatory markers. We also performed a Cox regression analysis to determine the association of NGAL with predefined clinical outcomes. RESULTS: The median value of NGAL was 50.5 ng/mL (IR 47.6-54.9 ng/mL), and higher NGAL values were recorded in diabetic patients. In a multiple linear regression model, including all univariate associates of NGAL, only log eGFR, log hs-CRP and log HDL cholesterol maintained an independent association with log NGAL. During the observational period, 30 patients died due to cardiovascular causes and 69 non-fatal CVE were registered. In the fully adjusted model, we observed a 2.08-fold increase in the risk of fatal CVE and a 1.50-fold increase in the risk of fatal and non-fatal CVE for each increment of 1 SD in log NGAL values. CONCLUSIONS: This is the first study that shows that serum NGAL is associated with cardiovascular events (fatal and non-fatal) in patients with CKD, independently of traditional risk factors, renal function and inflammation.

Serum uric acid may predict development of progressive acute kidney injury after open heart surgery.

OBJECTIVES: Acute kidney injury (AKI) is a common complication of cardiac surgery developing in 25-35% cases. Recently, neutrophil gelatinase-associated lipocalin (NGAL) was shown to predict AKI development earlier than serum creatinine. Some studies demonstrated the predictive role of post-operative serum uric acid (SUA) as an early marker of AKI. We aimed to study the role of serum and urine NGAL as well as SUA to predict progression of AKI. DESIGN AND METHODS: This is a prospective observational study of patients undergoing cardiac surgery. Blood and urine samples for measurement of uric acid, serum and urine NGAL levels were collected prior to cardiac surgery (0 h), and in the time course at 2nd and 24th hours after surgery. Patients who developed AKI were divided into two subgroups as progressing and non-progressing AKI. RESULTS: Sixty patients (42 males, 18 females) were included. After cardiac surgery, 40 patients developed AKI, 20 of whom non-progressing AKI, and 20 progressing AKI. All of the markers significantly increased in AKI patients. A receiver operator characteristics (ROC) curve analysis showed higher predictive ability of SUA for progressing AKI compared with serum and urine NGAL. When compared markers obtained at the second hour after surgery, UA had significantly large AUC than NGAL to predict AKI developed at 24 and 48 h, particularly in patients, who require renal replacement therapy (RRT). CONCLUSION: Uric acid seems to predict the progression of AKI and RRT requirement in patients underwent cardiac surgery better than NGAL.

The relationship between uric acid and erectile dysfunction in hypertensive subjects.

BACKGROUND: Endothelial dysfunction plays a major role in erectile dysfunction (ED). Uric acid (UA) is a marker of endothelial dysfunction. We hypothesized that increased UA levels may be associated with ED and aimed to investigate whether there is a relationship between, UA and ED in hypertensive patients. METHODS: A total of 200 hypertensive patients who have a normal treadmill exercise test were divided into two groups based on the Sexual Health Inventory for Men (SHIM) test (< 21 defined as ED n = 110, and ≥ 21 defined as normal erectile function n = 90). The differences between the ED and normal erectile function groups were compared and determinants of ED were analyzed. MAIN RESULTS: The prevalence of ED was found to be 55.0%. Office blood pressure level was comparable between groups. UA levels were significantly increased in the ED group (6.20 ± 1.56 vs 5.44 ± 1.32, p = 0.01). In a regression model, age [odds ratio (95% confidence interval): 1.08 (1.04-1.14), p = 0.001], smoking [odds ratio: 2.33 (1.04-5.20), p = 0.04] and UA [odds ratio: 1.76 (1.28-2.41), p = 0.04] were independent determinants of ED. An UA level of > 5.2 mg/dl had 76.2% sensitivity, 43.7% specificity, 62.9% positive and 59.4% negative predictive value for determining ED. CONCLUSION: UA is an independent determinant of ED irrespective of blood pressure control and questioning erectile function for hypertensive patients with increased UA levels may be recommended.

Allopurinol as a kidney-protective, cardioprotective, and antihypertensive agent: hype or reality?

Numerous experimental and clinical studies suggest that uric acid might have pathobiologic implications in the development and progression of hypertension, kidney disease, and coronary heart disease, among others, resulting in renewed interest in uric acid as a potential pathogenic mediator in these clinical conditions. Despite encouraging animal studies showing beneficial roles of allopurinol, clinical studies and randomized controlled trials remain scarce, and, despite available clinical evidence supporting a therapeutic role for allopurinol, multiple issues remain before routine use of allopurinol can be recommended for use in patients with hyperuricemia and hypertension, kidney disease, or coronary heart disease. These include a need for more robust clinical trial data that evaluate efficacy on hard clinical outcomes, optimal dose, duration of treatment, and the potential for serious allergic reactions. In this article we review the current available evidence describing the effects of allopurinol in hypertension, kidney disease, and coronary heart disease, highlighting unresolved issues surrounding allopurinol use for uric acid lowering in individuals without gout.

Uric acid as a potential mediator of cardiovascular morbidity in obstructive sleep apnea syndrome.

BACKGROUND AND AIMS: Obstructive sleep apnea (OSA) is now considered as an independent risk factor for cardiovascular (CV) disease. Although uric acid is increasingly being implicated in CV morbidity and mortality, no study attempted to determine independent role of uric acid in CV morbidity of OSA patients. We aimed to assess the role of serum uric acid as a potential mechanism of CV morbidity in a nonselected cohort of OSA patients. METHODS: This was a cohort study in which patients who had undergone a formal sleep study for diagnosis of OSA were recruited. Included patients were grouped according to apnea-hypopnea index (AHI) as mild, moderate and severe OSA. Patients with AHI<5 served as control group. Patients were interrogated as to cardiovascular morbid conditions which included prior history and an established diagnosis of coronary artery disease, cerebrovascular accident, congestive heart failure due to coronary artery disease and arrhythmias. RESULTS: 436 OSA patients included (72 controls, 97 with mild, 75 with moderate, and 192 with severe OSA). The severe group also had higher serum uric acid level compared with the control and other OSA groups. Linear regression showed that the Ln uric acid was positively associated with Ln AHI score. In unadjusted logistic regression, severe OSA was associated with higher odds of a cardiovascular event, OR=2.81 (1.307-6.041), p=0.0081 while the other categories of sleep apnea were not. However, severe OSA was no longer significant after adjusting for age, gender, diabetes mellitus status, hypertension status, BMI, and smoking, OR=1.882 (0.826-4.287), p=0.1322. Uric acid was significantly higher in those who had a cardiovascular event even in the mild, moderate and severe OSA groups. CONCLUSION: Hyperuricemia is strongly associated with cardiovascular disease in OSA patients. This strong relationship persists even after controlling for well-known traditional risk factors for cardiovascular disease.

The relationship between IL-10 levels and cardiovascular events in patients with CKD.

BACKGROUND AND OBJECTIVES: Cardiovascular disease is the leading cause of death in patients with CKD. IL-10 is considered an antiatherosclerotic cytokine. However, previous studies have failed to observe an association between IL-10 and cardiovascular disease in CKD. This study aimed to evaluate whether serum IL-10 levels were associated with the risk of cardiovascular events in CKD patients. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: Four hundred three patients with stages 1-5 CKD were followed for a mean of 38 (range=2-42) months for fatal and nonfatal cardiovascular events. IL-10 and IL-6 were measured at baseline together with surrogates of endothelial function (flow-mediated dilatation) and proinflammatory markers (high-sensitivity C-reactive protein and pentraxin-3). The association between IL-10 and flow-mediated dilatation through linear regression analyses was evaluated. The association between IL-10 and the risk of cardiovascular events was assessed with Cox regression analysis. RESULTS: IL-10, IL-6, high-sensitivity C-reactive protein, and pentraxin-3 levels were higher among participants with lower eGFR. Both fatal (25 of 200 versus 6 of 203 patients) and combined fatal and nonfatal (106 of 200 versus 23 of 203 patients) cardiovascular events were more common in patients with IL-10 concentration above the median. Flow-mediated dilatation was significantly lower in patients with higher serum IL-10 levels, but IL-10 was not associated with flow-mediated dilatation in multivariate analysis. Kaplan-Meier survival curves showed that patients with IL-10 below the median value (<21.5 pg/ml) had higher cumulative survival compared with patients who had IL-10 levels above the median value (log-rank test, P<0.001). CONCLUSIONS: IL-10 levels increase along with the reduction of kidney function. Higher serum IL-10 levels were associated with the risk of cardiovascular events during follow-up. We speculate that higher IL-10 levels in this context signify an overall proinflammatory milieu.

Neutrophil gelatinase-associated lipocalin in prediction of mortality in patients with hepatorenal syndrome: a prospective observational study.

BACKGROUND & AIMS: Hepatorenal syndrome (HRS) is a severe complication of cirrhosis which is characterized by renal dysfunction and associated with poor survival. Neutrophil gelatinase-associated lipocalin (NGAL) is a troponin-like biomarker for human acute kidney injury. We aimed to investigate levels of plasma and urine NGAL in HRS and predictive ability of these markers for all-cause mortality, in HRS, stable cirrhosis and control subjects. METHODS: A total of 64 patients with cirrhosis (8 patients with type 1 HRS, 22 with type 2 HRS, and 34 without HRS) and 23 control subjects were included in the study. Blood and urine samples were measured with Human NGAL sandwich ELISA. Patients were followed up prospectively. RESULTS: Patients with type 1 and type 2 HRS had significantly higher plasma and urine NGAL levels compared with stable cirrhosis and control subjects. Cox regression analysis showed that plasma NGAL and MELD-Na scores were independent predictors of mortality. ROC-curve analysis showed that the plot of the plasma NGAL, urine NGAL, MELD-Na and Child-Turcot-Pugh score could predict all-cause mortality in cirrhotic patients' area under the curve (AUC 0.819, 0.686, 0.807 and 0.795 respectively). CONCLUSIONS: NGAL could predict mortality in patients with HRS independent of other commonly used risk factors.

Thrombotic thrombocytopenic purpura secondary to ABO group incompatible blood transfusion in a patient after cardiac surgery.

The triggers of secondary thrombotic thrombopcytopenic purpura (TTP) include drug toxicity, radiation and high-dose chemotherapy, angioinvasive infections, surgery and acute graft versus host disease. TTP secondary to surgery have been reported in a number of cases. Most of the cases have been occurred after open heart surgery. Extensive endothelial damage is held responsible as the initiating mechanism in postoperative TTP cases. However, there is no report of secondary TTP describing development owing to ABO incompatible blood transfusion. Here, we describe a patient who developed TTP after transfusion of ABO incompatible blood during hospitalization for bypass surgery. We also propose a hypothesis which may account for the possible underlying mechanism.

Soluble TWEAK independently predicts atherosclerosis in renal transplant patients.

BACKGROUND: Cardiovascular risk is increased in the early stages of chronic kidney disease (CKD) and also found to be ongoing in renal transplant (Rtx) patients. As a sign of atherosclerosis, increased carotid intima-media thickness (CIMT) has been widely accepted as a strong predictor of cardiovascular disease (CVD) and mortality in CKD patients. A novel markers, soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) and neutrophil-to-lymphocyte ratio (NLR) were introduced as potential markers in inflammatory disorders including CKD. The role of Rtx in terms of atherogenesis is still unclear. We aimed to investigate the relationship between sTWEAK, NLR and CIMT in Rtx patients without overt CVD and to compare these results with those obtained from healthy subjects. METHODS: Cross-sectional analysis in which CIMT measurements, NLR and serum TWEAK levels were assessed in 70 Rtx patients (29 females; mean age, 40.6 ± 12.4 years) and 25 healthy subjects (13 females, mean age; 37.4±8.8 years). RESULTS: sTWEAK levels were significantly decreased (p=0.01) and hs-CRP, NLR and CIMT levels of Rtx patients were significantly increased compared to healthy subjects (p<0.0001, p=0.001, p<0.0001, respectively). sTWEAK was also found to be decreased when eGFR was decreased (p=0.04 between all groups). CIMT was positively correlated with sTWEAK and NLR in Rtx patients (r=0.81, p<0.0001 and r=0.33, p=0.006, respectively). sTWEAK was also positively correlated with NLR (r=0.37, p=0.002). In the multivariate analysis only sTWEAK was found to be an independent variable of increased CIMT. CONCLUSION: sTWEAK might have a role in the pathogenesis of ongoing atherosclerosis in Rtx patients.

Glomerulonephritis associated with tuberculosis: a case report and literature review.

Rapidly progressive glomerulonephritis caused mycobacterium tuberculosis is rare; however, three case have been reported to date. Crescentic glomerulonephritis is a life-threatening disease and together with the presence of tuberculous infection is associated with a poor outcome if treatment is inadequate and delayed. We describe the case of a 31-year-old female patient with nephrotic syndrome and progressive renal failure secondary to pulmonary tuberculosis. Renal biopsy showed crescent formation in 14 out of 27 glomeruli, and there was diffuse linear staining of immunoglobulin G deposits. Treatment included corticosteroids in combination with antituberculosis drugs for 2 months, and resulted in a significant improvement in renal function, the disappearance of proteinuria and pulmonary symptoms. We also present a review of the pertinent literature and discuss the pathophysiology of tuberculosis-related acute postinfectious glomerulonephritis.