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Interstitial nephritis [keywords]
- Kidney disease and risk of venous thromboembolism:a nationwide population-based case-control study. [JOURNAL ARTICLE]
- J Thromb Haemost 2014 Jul 10.
Chronic kidney disease is associated with hemostatic derangements, including both procoagulant activity and platelet dysfunction, which may influence the risk of venous thromboembolism. However, data associating kidney disease with risk of venous thromboembolism are sparse OBJECTIVES: We examined whether kidney disease is associated with increased risk of venous thromboembolism METHODS: We conducted this nationwide case-control study using data from medical databases. We included 128,096 patients with a hospital diagnosis of VTE in Denmark between 1980 and 2010 (54,473 had pulmonary embolism and 73,623 had deep venous thrombosis only) and 642,426 age-and gender-matched population controls based on risk-set sampling We identified all previous hospital diagnoses of kidney disease including nephrotic syndrome, glomerulonephritis without nephrotic syndrome, hypertensive nephropathy, chronic pyelonephritis/interstitial nephritis, polycystic kidney disease, diabetic nephropathy, or other kidney diseases. We used conditional logistic regression models to compute odds ratios (ORs) for venous thromboembolism with adjustment for potential confounders RESULTS: Kidney disease was associated with an adjusted OR for venous thromboembolism ranging from 1.41 (95% CI: 1.22-1.63) for hypertensive nephropathy to 2.89 (95% CI: 2.26-3.69) for patients with nephrotic syndrome. The association was strongest within the first three months after a diagnosis of chronic kidney disease (adjusted OR for nephrotic syndrome = 23.23, 95% CI: 8.58-62.89), gradually declining thereafter. The risk, however, remained elevated for more than five years, especially in patients with nephrotic syndrome and glomerulonephritis CONCLUSIONS: Kidney diseases, in particular nephrotic syndrome and glomerulonephritis, were associated with an increased risk of venous thromboembolism This article is protected by copyright. All rights reserved.
- A Patient With Minimal Change Disease and Acute Focal Tubulointerstitial Nephritis Due To Traditional Medicine: A Case Report and Small Literature Review. [JOURNAL ARTICLE]
- Explore (NY) 2014 Jun 16.
Gongjin-dan (GJD) is a traditional formula that is widely used in Korea and China, and it has been used from 1345 AD in China to improve the circulation between the kidneys and the heart and to prevent all diseases. However, its adverse effects have not yet been reported. We present a patient with minimal change disease and focal tubulointerstitial nephritis associated with GJD. A 72-year-old man visited the clinic for generalized edema 20 days after starting GJD. His serum albumin level was low and nephrotic-range proteinuria was detected. A kidney biopsy showed minimal change disease and acute tubulointerstitial nephritis. After stopping GJD, a spontaneous complete remission was achieved. We discuss the possible pathogenesis of GJD-induced minimal change disease and review the adverse effects of GJD's ingredients and traditional Chinese medicines that can induce proteinuria. We report a new adverse effect of GJD, which might induce increased IL-13 production and an allergic response, leading to minimal change disease and focal tubulointerstitial nephritis.
- [Acute kidney injury in children]. [English Abstract, Journal Article]
- Srp Arh Celok Lek 2014 May-Jun; 142(5-6):371-7.
Acute kidney injury (AKI) is a clinical condition considered to be the consequence of a sudden decrease (> 25%) or discontinuation of renal function. The term AKI is used instead of the previous term acute renal failure, because it has been demonstrated that even minor renal lesions may cause far-reaching consequences on human health. Contemporary classifications of AKI (RIFLE and AKIN) are based on the change of serum creatinine and urinary output. In the developed countries, AKI is most often caused by renal ischemia, nephrotoxins and sepsis, rather than a (primary) diffuse renal disease, such as glomerulonephritis, interstitial nephritis, renovascular disorder and thrombotic microangiopathy. The main risk factors for hospital AKI are mechanical ventilation, use of vasoactive drugs, stem cell transplantation and diuretic-resistant hypervolemia. Prerenal and parenchymal AKI (previously known as acute tubular necrosis) jointly account for 2/3 of all AKI causes. Diuresis and serum creatinine concentration are not early diagnostic markers of AKI. Potential early biomarkers of AKI are neutrophil gelatinase-associated lipocalin (NGAL), cystatin C, kidney injury molecule-1 (KIM-1), interleukins 6, 8 and 18, and liver-type fatty acid-binding protein (L-FABP). Early detection of kidney impairment, before the increase of serum creatinine, is important for timely initiated therapy and recovery. The goal of AKI treatment is to normalize the fluid and electrolyte status, as well as the correction of acidosis and blood pressure. Since a severe fluid overload resistant to diuretics and inotropic agents is associated with a poor outcome, the initiation of dialysis should not be delayed. The mortality rate of AKI is highest in critically ill children with multiple organ failure and hemodynamically unstable patients.
- Prognostic value of glomerular C4d staining in patients with IgA nephritis. [Journal Article]
- Int J Clin Exp Pathol 2014; 7(6):3299-304.
Mesangial IgA deposition is the initiative factor in the pathogenesis of IgA nephropathy (IgAN). Glomerular IgA depositon leads to activation local complement system. C4d positivity shows that complement activation occurs via alternative pathway. C4d positivity at the time of renal biopsy can be associated with poor prognosis in IgA nephropathy. We aimed to evaluate C4d deposition and renal outcome in patients with IgA nephritis.Between January 2005 and December 2009, 40 patients with IgA nephritis were enrolled. Renal biopsy specimens of 33 patients have been evaluated. C4d immunohistochemical staining was performed 3-μm deparaffinized and rehydrated sections of formaldehyde-fixed renal tissues, using rabbit polyclonal anti-human C4d as the antibody. Baseline demographical, clinical and laboratory data were recorded retrospectively.Mean age of the patients was 35.9 ± 12.9 years and female/male ratio was 19/21. Mean duration of follow-up was 32.8 (12-60) months. Baseline glomerular filtration ratio (GFR) and proteinuria were 55.8 ml/min and 2.44 gr/day respectively at the time of renal biopsy. Eleven patients were C4d positive. Presence of hypertension (p=0.133), proteinuria (p=0.007), serum creatinine levels (p=0.056) and glomerulosclerosis (p=0.004), mesengial hypersellularity (p=0.0001) and interstitial fibrosis (p=0.006) at the time of renal biopsy were higher in C4d positive group rather than negative group. Evolution to renal failure were 63.6% in C4d positive group and 13.6% in negative group (p=0.006). Renal survival at 3 years was 39% in C4d-positive patients versus 66.7% in the C4d-negative patients (log rank- p=0.0072).
- Mononuclear Phagocyte Accumulation in Visceral Tissue in HIV Encephalitis: Evidence for Increased Monocyte/Macrophage Trafficking and Altered Differentiation. [JOURNAL ARTICLE]
- Curr HIV Res 2014 Jul 13.
The invasion of circulating monocytes/macrophages (Mφ)s from the peripheral blood into the central nervous system (CNS) appears to play an important role in the pathogenesis of HIV dementia (HIV-D), the most severe form of HIV-associated neurocognitive disorders (HAND), often confirmed histologically as HIV encephalitis (HIVE). In order to determine if trafficking of monocytes/Mφs is exclusive to the CNS or if it also occurs in organs outside of the brain, we have focused our investigation on visceral tissues of patients with HIVE. Liver, lymph node, spleen, and kidney autopsy tissues from the same HIVE cases investigated in earlier studies were examined by immunohistochemistry for the presence of CD14, CD16, CD68, Ki-67, and HIV-1 p24 expression. Here, we report a statistically significant increase in accumulation of Mφs in kidney, spleen, and lymph node tissues in specimens from patients with HIVE. In liver, we did not observe a significant increase in parenchymal macrophage accumulation, although perivascular macrophage accumulation was consistently observed with nodular lesions in 4 of 5 HIVE cases. We also observed an absence of CD14 expression on splenic Mφs in HIVE cases, which may implicate the spleen as a potential source of increased plasma soluble CD14 in HIV infection. HIV-1 p24 expression was observed in liver, lymph node and spleen but not kidney. Interestingly, renal pathology suggestive of chronic tubulointerstitial nephritis (possibly due to chronic pyelonephritis), including tubulointerstitial scarring, chronic interstitial inflammation and focal global glomerulosclerosis, without evidence of HIV-associated nephropathy (HIVAN), was seen in four of eight HIVE cases. Focal segmental and global glomerulosclerosis with tubular dilatation and prominent interstitial inflammation, consistent with HIVAN, was observed in two of the eight cases. Abundant cells expressing monocyte/Mφ cell surface markers, CD14 and CD68, were also CD16+ and found surrounding dilated tubules and adjacent to areas of glomerulosclerosis. The finding of co-morbid HIVE and renal pathology characterized by prominent interstitial inflammation may suggest a common mechanism involving the invasion of activated monocytes/Mφs from circulation. Monocyte/Mφ invasion of visceral tissues may play an important role in the immune dysfunction as well as comorbidity in AIDS and may, therefore, provide a high value target for the design of therapeutic strategies.
- The contribution of epithelial-mesenchymal transition to renal fibrosis differs among kidney disease models. [JOURNAL ARTICLE]
- Kidney Int 2014 Jul 9.
The impact of the epithelial-mesenchymal transition (EMT) to the formation of renal fibrosis has been debated in several lineage-tracing studies, with conflicting findings. Such disparities may have arisen from varying experimental conditions such as different disease models, the mouse strain, and type of genetic alteration used. In order to determine the contribution of these factors to EMT, we generated four kidney disease models in several mouse strains genetically modified to express enhanced green fluorescence protein (EGFP) in cortical tubular epithelial cells under the control of the γ-glutamyl transpeptidase promoter. Using this approach, the EMT was visible and quantifiable based on a count of EGFP-positive interstitial cells in the fibrotic kidney sections of the four renal disease models found to be either EMT-prone or -resistant. The EMT-prone models consisted of unilateral ureteral obstruction and ischemic nephropathy in SJL mice. The EMT-resistant models consisted of ureteral obstruction in C57B/6 and F1(C57B/6 × SJL) mice, adriamycin nephrosis in 129 mice, and nephrotoxic serum nephritis in SJL mice. Analyses of these renal disease models suggest the emergence of EMT-derived fibroblasts arises in a disease-specific and strain-dependent manner. Thus, when considering molecular mechanisms and involvement of the EMT in renal fibrosis, it is important to take into account the experimental conditions, particularly the mouse strain and type of disease model.Kidney International advance online publication, 9 July 2014; doi:10.1038/ki.2014.235.
- Tubulointerstitial nephritis complicating IVIG therapy for X-linked agammaglobulinemia. [JOURNAL ARTICLE]
- BMC Nephrol 2014 Jul 8; 15(1):109.
Patients with X-linked agammaglobulinemia (XLA) develop immune-complex induced diseases such as nephropathy only rarely, presumably because their immunoglobulin (Ig) G concentration is low. We encountered a patient with XLA who developed tubulointerstitial nephritis during treatment with intravenous immunoglobulin (IVIG).A 20-year-old man was diagnosed with XLA 3 months after birth and subsequently received periodic gamma-globulin replacement therapy. Renal dysfunction developed at 19 years of age in association with high urinary beta2-microglobulin (MG) concentrations. A renal biopsy specimen showed dense CD3-positive lymphocytic infiltration in the tubulointerstitium and tubular atrophy, while no IgG4-bearing cell infiltration was found. Fibrosclerosis and crescent formation were evident in some glomeruli. Fluorescent antibody staining demonstrated deposition of IgG and complement component C3 in tubular basement membranes. After pulse steroid therapy was initiated, urinary beta2-MG and serum creatinine concentrations improved.Neither drug reactions nor collagen disease were likely causes of tubular interstitial disorder in this patient. Although BK virus was ruled out, IgG in the gamma-globulin preparation might have reacted with a pathogen present in the patient to form low-molecular-weight immune complexes that were deposited in the tubular basement membrane.
- Non-diabetic renal diseases in a multi-ethnic New Zealand cohort with type 2 diabetes mellitus: clinical and histopathological features. [JOURNAL ARTICLE]
- Pathology 2014 Jun 20.
The aims of this study were to identify non-diabetic renal disease (NDRD), including obesity related glomerulopathy (ORG) in diabetic patients, and compare the findings with those of pure diabetic nephropathy (DN).Ninety-three renal biopsies from diabetic patients were reviewed retrospectively, along with their clinical findings at biopsy and their estimated glomerular filtration rate (eGFR) over 5 years follow-up. DN and focal segmental glomerulosclerosis (FSGS) were diagnosed on blinded histology review, together with assessment of renal compartment histology. Other NDRD were diagnosed on full review.Most patients were obese with poor renal function at biopsy. NDRD occurred in more than two-thirds of biopsies. FSGS and interstitial nephritis were common. Patients with pure FSGS presented earlier, and had favourable histological features and clinical course. Most FSGS patients fulfilled criteria for ORG. Biopsies with interstitial nephritis showed more functional glomerular tissue, and most patients retained good renal function. Adverse prognostic features were DN versus NDRD, nodular grade of DN, low eGFR at biopsy, and severe chronic histological changes.In this population, ORG mechanisms contribute to renal injury. FSGS is frequent, and should be diagnosed separately from any DN. Biopsy to confirm suspicion of interstitial nephritis should be performed even if retinopathy is present.
- Hepatitis C virus associated glomerulopathies. [REVIEW]
- World J Gastroenterol 2014 Jun 28; 20(24):7544-7554.
Hepatitis C virus (HCV) infection is a systemic disorder which is often associated with a number of extrahepatic manifestations including glomerulopathies. Patients with HCV infection were found to have a higher risk of end-stage renal disease. HCV positivity has also been linked to lower graft and patient survivals after kidney transplantation. Various histological types of renal diseases are reported in association with HCV infection including membranoproliferative glomerulonephritis (MPGN), membranous nephropathy, focal segmental glomerulosclerosis, fibrillary glomerulonephritis, immunotactoid glomerulopathy, IgA nephropathy, renal thrombotic microangiopathy, vasculitic renal involvement and interstitial nephritis. The most common type of HCV associated glomerulopathy is type I MPGN associated with type II mixed cryoglobulinemia. Clinically, typical renal manifestations in HCV-infected patients include proteinuria, microscopic hematuria, hypertension, acute nephritis and nephrotic syndrome. Three approaches may be suggested for the treatment of HCV-associated glomerulopathies and cryoglobulinemic renal disease: (1) antiviral therapy to prevent the further direct damage of HCV on kidneys and synthesis of immune-complexes; (2) B-cell depletion therapy to prevent formation of immune-complexes and cryoglobulins; and (3) nonspecific immunosuppressive therapy targeting inflammatory cells to prevent the synthesis of immune-complexes and to treat cryoglobulin associated vasculitis. In patients with moderate proteinuria and stable renal functions, anti-HCV therapy is advised to be started as pegylated interferon-α plus ribavirin. However in patients with nephrotic-range proteinuria and/or progressive kidney injury and other serious extra-renal manifestations, immunosuppressive therapy with cyclophosphamide, rituximab, steroid pulses and plasmapheresis should be administrated.
- Inflammatory pseudotumors of the kidney due to IgG4-related tubulointerstitial nephritis. [Journal Article]
- Rom J Morphol Embryol 2014; 55(2):419-23.
The paper presents the case of a female patient who was admitted to our department because of prolonged febrile syndrome, altered general status and renal tumoral masses revealed by thoracic and abdominal CT. After thorough histological examination, including immunohisto-chemistry and in situ hybridization studies, we reached the diagnosis of renal pseudotumoral masses due to IgG4-related tubulointerstitial nephritis. The kidney is a distinct target organ affected by IgG4-related sclerosing disease, and the most frequent manifestation is tubulo-interstitial nephritis. We described the clinical, imagistic and histopathological features of kidney and urological involvement in IgG4-related sclerosing disease, especially focusing on IgG4-related tubulointerstitial nephritis. This is a rare case of IgG4-related sclerosing disease without extrarenal features, excepting lumboaortic lymphadenopathy.