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Interstitial nephritis [keywords]
- The Value of Measuring Urinary β2-Microglobulin and Serum Creatinine for Detecting Tubulointerstitial Nephritis and Uveitis Syndrome in Young Patients With Uveitis. [JOURNAL ARTICLE]
- JAMA Ophthalmol 2014 Oct 30.
Tubulointerstitial nephritis and uveitis (TINU) syndrome is characterized by tubulointerstitial and ocular inflammation. Thus far, the value of noninvasive diagnostic tests is not known.To determine whether urinary β2-microglobulin (β2M), urinary protein, and serum creatinine have predictive value for detecting TINU syndrome in young patients with uveitis.This prospective cohort study was conducted July 2010 through February 2013 at a tertiary care referral center in Utrecht, the Netherlands. Forty-five consecutive new patients with uveitis aged 22 years or younger were enrolled.Urinary β2M, urinary protein, and serum creatinine were measured prospectively, and the estimated glomerular filtration rate was calculated.A post hoc analysis was performed to determine whether urinary β2M, urinary protein, serum creatinine, estimated glomerular filtration rate, and/or pyuria were correlated with definitive and probable cases of TINU syndrome.Eighteen of the 45 patients (40%) in our cohort had elevated urinary β2M levels, and 10 patients (22%) had elevated serum creatinine levels. Twenty of 43 patients (47%) had proteinuria. Eight of the 45 patients were diagnosed by a pediatric nephrologist as having renal dysfunction that suggested acute interstitial nephritis. Of these 8 patients, 2 were definitively diagnosed as having TINU syndrome (confirmed by renal biopsy). After excluding other causes of renal dysfunction, the remaining 6 patients with uveitis and renal dysfunction fulfilled the criteria of probable TINU syndrome. The 8 patients with definitive or probable TINU syndrome had higher urinary β2M levels than patients with normal renal function (median β2M, 1.95 mg/L; 95% CI, 1.26-5.16 mg/L vs 0.20 mg/L; 95% CI, 0.19-0.21 mg/L; P < .001; Mann-Whitney U test). Our analysis revealed that the positive predictive value of increased β2M combined with increased serum creatinine was 100% for detecting definitive and/or probable TINU syndrome.These data suggest that urinary β2M and serum creatinine levels are sensitive and relatively simple diagnostic screening tools for detecting renal dysfunction to diagnose TINU syndrome in young patients with uveitis similar to those evaluated in this study.
- Pure Motor Axonal Neuropathy, Organomegaly, Impaired Glucose Tolerance, M Protein, Skin Changes, Multiple Plasmacytomas & Acute Interstitial Nephritis in Osteolytic Myeloma: Beyond POEMS! [Journal Article]
- Indian J Hematol Blood Transfus 2014 Sep; 30(Suppl 1):115-9.
The authors describe a case of 52-year-old male who presented with sudden onset deterioration of weakness of both lower limbs and retention of urine. He had 1 month history of gradually progressive weakness of legs. On examination, there were lower motor neuron signs in lower extremity, digital clubbing and a lump over left iliac fossa. Routine blood tests showed impaired glucose tolerance, confirmed by oral glucose tolerance test while renal parameters were normal. Magnetic resonance imaging of spine documented osteolytic lesions, long segment epidural mass in thoracic spine and a mass overlying the left iliac bone, both were revealed to be plasmacytoma following cytology. Ultrasonography of abdomen showed splenomegaly. Nerve conduction studies showed gross axonal, motor, asymmetric polyneuropathy with conduction block involving all the four extremities, mainly lower limbs with sensory sparing. Serum protein electrophoresis showed M spike, and bone marrow showed diffuse neoplastic plasma cell proliferation. Osteolytic lesion was present in skull radiograph. Then in the course of illness the patient developed acute renal failure due to acute interstitial nephritis as evidenced from proteinuria and kidney biopsy, which improved with steroids and chemotherapy but unfortunately we lost the patient after 2 weeks of initiation of chemotherapy.
- Sarcoidosis in native and transplanted kidneys: incidence, pathologic findings, and clinical course. [Journal Article]
- PLoS One 2014; 9(10):e110778.
Renal involvement by sarcoidosis in native and transplanted kidneys classically presents as non caseating granulomatous interstitial nephritis. However, the incidence of sarcoidosis in native and transplant kidney biopsies, its frequency as a cause of end stage renal disease and its recurrence in renal allograft are not well defined, which prompted this study. The electronic medical records and the pathology findings in native and transplant kidney biopsies reviewed at the Johns Hopkins Hospital from 1/1/2000 to 6/30/2011 were searched. A total of 51 patients with a diagnosis of sarcoidosis and renal abnormalities requiring a native kidney biopsy were identified. Granulomatous interstitial nephritis, consistent with renal sarcoidosis was identified in kidney biopsies from 19 of these subjects (37%). This is equivalent to a frequency of 0.18% of this diagnosis in a total of 10,023 biopsies from native kidney reviewed at our institution. Follow-up information was available in 10 patients with biopsy-proven renal sarcoidosis: 6 responded to treatment with prednisone, one progressed to end stage renal disease. Renal sarcoidosis was the primary cause of end stage renal disease in only 2 out of 2,331 transplants performed. Only one biopsy-proven recurrence of sarcoidosis granulomatous interstitial nephritis was identified.Renal involvement by sarcoidosis in the form of granulomatous interstitial nephritis was a rare finding in biopsies from native kidneys reviewed at our center, and was found to be a rare cause of end stage renal disease. However, our observations indicate that recurrence of sarcoid granulomatous inflammation may occur in the transplanted kidney of patients with sarcoidosis as the original kidney disease.
- Changes in the aetiology, clinical presentation and management of acute interstitial nephritis, an increasingly common cause of acute kidney injury. [REVIEW]
- Nephrol Dial Transplant 2014 Oct 16.
Acute interstitial nephritis (AIN) is an important cause of acute kidney injury that has experienced significant epidemiological and clinical changes in the last years. The classical presentation, mostly induced by antibiotics and accompanied by evident hypersensitivity manifestations (skin rash, eosinophilia, fever) has been largely replaced by oligosymptomatic presentations that require a higher index of suspicion and are increasingly recognized in the elderly, having non-steroidal anti-inflammatory agents and proton pump inhibitors as frequent offending drugs. Drug-induced AIN continues to be the commonest type, but it requires a careful differential diagnosis with other entities (tubulointerstitial nephritis with uveitis syndrome, IgG4-related disease, drug reaction with eosinophilia and systemic symptom syndrome, sarcoidosis and other systemic diseases) that can also induce AIN. Cortico-dependant, relapsing AIN is a recently recognized entity that poses an important therapeutic challenge. Although corticosteroids are widely used in drug-induced AIN to speed kidney function recovery and avoid chronic kidney disease, their efficacy has not been tested by randomized controlled trials. New diagnostic tests and biomarkers, as well as prospective therapeutic studies are needed to improve AIN diagnosis and management.
- Granulomatous tubulointerstitial nephritis secondary to omeprazole. [Journal Article]
- BMJ Case Rep 2014.
Drug-induced interstitial nephritis is a common cause of acute kidney injury indicated by elevated serum creatinine. We report a case of omeprazole-induced acute granulomatous interstitial nephritis (GIN). Our patient developed acute GIN secondary to omeprazole ingestion requiring haemodialysis. Treatment with steroids and withdrawal of omperazole was successful allowing the patient to discontinue haemodialysis in 3 months. She remains dialysis free with chronic kidney disease stage IV, reflected by a serum creatine of 191 μmol/L and estimated glomerular filtration rate of 23 mL/min/1.73 m(2) at 5 years on follow-up.
- Characteristics and clinical outcome of nonsteroidal anti-inflammatory drug-induced acute hepato-nephrotoxicity among Chinese patients. [Journal Article]
- World J Gastroenterol 2014 Oct 14; 20(38):13956-65.
To determine the clinicopathological characteristics of nonsteroidal anti-inflammatory drug (NSAID)-induced acute hepato-nephrotoxicity among Chinese patients.We conducted a retrospective chart review of patients using the International Classification of Diseases, Ninth Revision diagnosis code for acute kidney injury (AKI) (584.5 or 584.9) and for acute liver injury (ALI) (570.0 or 573.3) from January 2004 to December 2013. Medical records were reviewed to confirm the diagnosis of AKI and ALI and to quantify NSAID administration.Seven of 59 patients (11.8%) were identified with acute hepato-nephrotoxicity induced by NSAIDs. Five patients (71.4%) received over the recommended NSAIDs dose. Compared with NSAIDs-associated mere AKI, the risk factors of NSAIDs-induced acute hepato-nephrotoxicity are age older than 60 years (57.1%), a high prevalence of alcohol use (71.4%) and positive hepatitis B virus (HBV) markers (85.7%). Compared with NSAIDs-associated mere ALI, the risk factors of NSAIDs-induced acute hepato-nephrotoxicity are age older than 60 years (57.1%), increased extracellular volume depletion (71.4%), and renin-angiotensin-aldosterone system (RAAS) inhibitor combined use (57.1%). Acute interstitial nephritis and acute tubulointerstitial disease were apparent in three out of six (42.9%) kidney biopsy patients, respectively. Acute hepatitis was found in four out of six (66.7%) liver biopsy patients. Overall complete recovery occurred in four patients within a mean of 118.25 ± 55.42 d.The injury typically occurred after an overdose of NSAIDs. The risk factors include age older than 60 years, alcohol use, positive HBV markers, extracellular volume depletion and RAAS inhibitor combined use.
- Renal interstitial mast cell counts differ across classes of proliferative lupus nephritis. [Journal Article]
- Folia Histochem Cytobiol 2014; 52(3):218-24.
Systemic lupus erythematosus frequently involves the kidneys leading to significant morbidity and mortality. It is classified according to glomerular involvement pattern but tubulointerstitial lesions are also important for progression and prognosis, as seen in other kidney glomerular diseases. One of the cell types which participate in this process are mast cells. The aim of the study was to analyze the counts of tryptase-positive and chymase-positive mast cells in lupus nephritis classes II, III and IV. Material consisted of 42 renal biopsies from patients with lupus nephritis; 11 class II, 9 class III and 22 class IV. Chymase- and tryptase-containing cells were stained by immunohistochemistry and counted microscopically. Mean count of chymase-positive mast cells was 9.8/10 high power fields (hpf) for the whole group, 4.66 for class II, 11.89 for class III, and 11.51 for class IV. The mean count of tryptase-positive cells was 18.6/10 hpf for the whole group, 7.65 for class II, 25.57 for class III, and 21.23 for class IV. The differences between lupus nephritis classes were significant both for chymase- and tryptase-positive cells. Tryptase- but not chymase-positive cell counts showed a correlation with the creatinine level (R = 0.35). These results suggest that mast cells are involved to a different degree in the pathogenesis of lupus nephritis depending on the class of the disease.
- The rs1800471 Polymorphism of TGFB1 Gene, Serum TGF-Beta1 Level and Chronic Kidney Disease Progression. [JOURNAL ARTICLE]
- Adv Exp Med Biol 2014 Oct 9.
The aim of the study was to investigate whether rs1800471 polymorphism in TGFB1 gene is associated with the development and progression of non-diabetic chronic kidney disease. Moreover, we examined the serum TGF-beta1 concentration and its association with that polymorphism and progression of the disease. We applied two different methodological approaches. Firstly, a family based study was carried out, comprised of 109 patients with non-diabetic chronic kidney disease and their 218 healthy parents, using the transmission/disequilibrium test. The rs1800471 polymorphism and serum TGF-beta1 level were determined in all subjects. Serum TGF-beta1 concentration was also measured in 40 healthy controls. Secondly, we performed a case-control orientated study to determine whether rs1800471 polymorphism and other factors influence the progression of renal impairment. We found no relationships between rs1800471 polymorphism allele transfer and the incidence or progression of non-diabetic chronic kidney disease. We found, however, that the serum TGF-beta1 was significantly higher in patients than in controls. In conclusion, rs1800471 polymorphism in TGFB1 gene does not have an impact on the development and progression of non-diabetic chronic kidney disease caused by primary glomerulopathy and chronic interstitial nephritis. The increased serum TGF-beta1 concentration in such patients suggests its role in the pathomechanism of the disease. Circulating TGF-beta1 level is determined in a multifactorial way, not by rs1800471 polymorphism in TGFB1 gene.
- [Pharmacogenetic aspects of candesartan application for the treatment of arterial hypertension in patients with chronic pyelonephritis]. [English Abstract, Journal Article]
- Lik Sprava 2014 Mar-Apr; (3-4):119-25.
Now necessity of the strict control arterial pressure (AP) is conventional at chronic diseases of kidneys. Inhibitors of receptors AT1R (BAR) are recognized all over the world as preparations of the first of some for treatment of renoparenchimal hypertensia. The purpose research--to study of clinical effect of Candesartan at patients with renoparenchimal hypertensia depending on a genotype. Survey 50 patients with inspected patients with renoparenchimal hypertensia on a background of chronic pyelonephritis, polymorphism of gene of angiotensin 11 of the first type is certain. Patients appointed Kandesartan in doses of 8-32 (Mg), observed in current of 12 months. By results of research the genotype AA is revealed at 46%, AC at 48%, CC at 6% of patients. Allel A it is revealed in a genotype of 94%, allel C - 54% of patients of renoparenchimal hypertensia. A target level the AP will reach at 94.,3% patients. Kandesartan has shown high clinical effect at all variants of polymorphism of gene AT1R.
- Lupus erythematosus tumidus: a unique disease entity. [Journal Article]
- Hawaii J Med Public Health 2014 Sep; 73(9 Suppl 1):18-21.
Lupus erythematosus tumidus (LET) is a photosensitive skin disease characterized by succulent, edematous, and non-scarring plaques. Histologic features include perivascular and periadnexal lymphocytic infiltration and interstitial mucin deposition. Despite being first described in 1909, there are few case reports in the current literature describing this disease and even fewer that discuss treatment. We describe a case of a 22-year-old woman with systemic lupus erythematosus (SLE) and secondary class V lupus nephritis. She was referred to Dermatology for an intermittent pruritic facial eruption that was clinically and histologically consistent with LET. There is much controversy in literature as to whether or not LET is a unique variant of cutaneous lupus erythematosus. Interestingly, the mainstay of treatment for LET, in the limited case reports and series that exist, is with antimalarial drugs, which our patient had already been taking for SLE. This case exemplifies the need for complete disease characterization, evidence-based treatment, and a multidisciplinary approach.