scholarly journals Biopsy-Proven Acute Tubular Necrosis due to Vancomycin Toxicity

2011 ◽  
Vol 2011 ◽  
pp. 1-4 ◽  
Author(s):  
Farheen Shah-Khan ◽  
Marc H. Scheetz ◽  
Cybele Ghossein
Keyword(s):  
Acute Kidney Injury ◽  
Interstitial Nephritis ◽  
Acute Tubular Necrosis ◽  
Kidney Injury ◽  
Acute Interstitial Nephritis ◽  
Etiologic Factor ◽  
Clinical Use ◽  
Tubular Necrosis

Vancomycin (VAN) has been associated with acute kidney injury (AKI) since it has been put into clinical use in the 1950's. Early reports of AKI were likely linked to the impurities of the VAN preparation. With the advent of the more purified forms of VAN, the incidence of AKI related to VAN were limited to acute interstitial nephritis (AIN) or as a potentiating agent to other nephrotoxins such as Aminoglycosides. VAN as the sole etiologic factor for nephrotoxic acute tubular necrosis (ATN) has not been described. Here, we report a case of biopsy-proven ATN resulting from VAN.

P0580ACUTE INTERSTITIAL NEPHRITIS RELATED TO EMPAGLIFLOZIN

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Alon Bnaya ◽  
Eyal Itzkowitz ◽  
Jawad Atrash ◽  
Mohsen Abu-Alfeilat ◽  
Linda Shavit
Keyword(s):  
Diabetes Mellitus ◽  
Acute Kidney Injury ◽  
Case Report ◽  
Interstitial Nephritis ◽  
Acute Tubular Necrosis ◽  
Kidney Injury ◽  
Acute Interstitial Nephritis ◽  
Sglt2 Inhibitors ◽  
Hemodynamic Changes ◽  
Tubular Necrosis

Abstract Background and Aims SGLT-2 inhibitors are effective anti-hyperglycemic agents with proved cardiovascular and renal benefits. However, there have been post marketing reports of episodes of acute kidney injury (AKI), some requiring hospitalization and even dialysis in patients receiving SGLT2 inhibitors. This phenomenon may be related to volume contraction and hemodynamic changes, particularly in patients with other risk factors (such as patients on RAAS blocking agents or NSAIDS, patients with CKD). We present a case of acute interstitial nephritis (AIN) and acute tubular necrosis related to an SGLT2-inhibitor. Method Case report description. Results A 67-year-old women was admitted with weakness, dizziness and abdominal pain. Her medical history was remarkable for hypertension, diabetes mellitus, ischemic heart disease and peripheral vascular disease. Her medications included bisoprolol, losartan, amlodipine, sitagliptin and aspirin. Two months prior the current presentation, empagliflozin was prescribed by her primary physician for her diabetes mellitus. However, several days after initiation of empgliflozin she felt weak and dizzy and empagliflozin was discontinued. A week before the current presentation, empagliflozin was re-initiated by her cardiologist. The patient reported no recent illness, fevers, rash, arthralgias, respiratory symptoms or bone pain. She denied exposure to other new medications (including NSAIDS and antibiotics). On admission, blood pressure was 165/76 mm Hg. The rest of the physical examination was unremarkable. Laboratory studies revealed acute kidney injury (creatinine 3.19 mg/dL, BUN 28 mg/dL, baseline creatinine 0.9 mg/dL). Complete blood count demonstrated no eosinophilia or thrombocytopenia. Urinalysis showed a few leukocytes but no red cells or casts. The urine protein to creatinine ratio was 5160 mg of protein per gram creatinine. Abdominal ultrasonography showed normal-size kidneys and no hydronephrosis. Immunologic and infectious serologies were unremarkable. over several days the patient became oligo-anuric and creatinine peaked to 9.22 mg/dL and hemodialysis was initiated. Empiric treatment with prednisone was given and a renal biopsy was performed. Four glomeruli were seen on light microscopy. The glomeruli were normocellular. An interstitial infiltrate of lymphocytes and small numbers of eosinophils were seen. Thining of the renal tubular brush border with intra-tubular necrotic content was a also seen. Immunofluorescence was negative. The findings were compatible with acute interstitial nephritis and acute tubular necrosis (Figure 1). The patient was discharged with a regimen of intermittent hemodialysis and steroid therapy. Three months later, urine output and kidney function improved, and the patient was weaned off dialysis. Conclusion In this case report, we describe previously unreported histologically proven AIN likely related to empagliflozin exposure. Although SGLT2 inhibitors have been reported to be associated with AKI it has been supposed to be related to volume contraction and hemodynamic changes. As virtually any drug can cause AIN, further proof of the drug's causation in our case was an onset of renal dysfunction with re- institution of empagliflozin, biopsy-proven AIN and absence of other drugs, infection or systemic disease that might cause AIN. With the dramatic increase in use of SGLT-2 inhibitors worldwide, treating physicians should be aware of AIN as a possible cause of AKI in this context.

scholarly journals Prognosis of Acute Kidney Injury and Hepatorenal Syndrome in Patients with Cirrhosis: A Prospective Cohort Study

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Andrew S. Allegretti ◽  
Guillermo Ortiz ◽  
Julia Wenger ◽  
Joseph J. Deferio ◽  
Joshua Wibecan ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Cohort Study ◽  
Prospective Cohort Study ◽  
Acute Tubular Necrosis ◽  
Prospective Cohort ◽  
Hepatorenal Syndrome ◽  
Kidney Injury ◽  
Multicenter Studies ◽  
Urinary Sediment ◽  
Tubular Necrosis

Background/Aims. Acute kidney injury is a common problem for patients with cirrhosis and is associated with poor survival. We aimed to examine the association between type of acute kidney injury and 90-day mortality.Methods. Prospective cohort study at a major US liver transplant center. A nephrologist’s review of the urinary sediment was used in conjunction with the 2007 Ascites Club Criteria to stratify acute kidney injury into four groups: prerenal azotemia, hepatorenal syndrome, acute tubular necrosis, or other.Results. 120 participants with cirrhosis and acute kidney injury were analyzed. Ninety-day mortality was 14/40 (35%) with prerenal azotemia, 20/35 (57%) with hepatorenal syndrome, 21/36 (58%) with acute tubular necrosis, and 1/9 (11%) with other (p=0.04overall). Mortality was the same in hepatorenal syndrome compared to acute tubular necrosis (p=0.99). Mortality was lower in prerenal azotemia compared to hepatorenal syndrome (p=0.05) and acute tubular necrosis (p=0.04). Ten participants (22%) were reclassified from hepatorenal syndrome to acute tubular necrosis because of granular casts on urinary sediment.Conclusions. Hepatorenal syndrome and acute tubular necrosis result in similar 90-day mortality. Review of urinary sediment may add important diagnostic information to this population. Multicenter studies are needed to validate these findings and better guide management.

Endocrine Summary

2014 ◽  
pp. 549-566
Author(s):  
Graham T. McMahon
Keyword(s):  
Acute Kidney Injury ◽  
Filtration Rate ◽  
Hospital Admissions ◽  
Kidney Injury ◽  
Acute Interstitial Nephritis ◽  
Hospitalized Patients ◽  
Acute Glomerulonephritis ◽  
Creatinine Concentration ◽  
Tubular Necrosis ◽  
Definition Of

Acute renal failure, now referred to as acute kidney injury (AKI), complicates 5–10% of general hospital admissions and is associated with increased morbidity and mortality and prolonged hospitalizations. The definition of AKI varies, but it is usually defined as an increase in serum creatinine concentration of 25–50% above the baseline, a decline in estimated glomerular filtration rate (eGFR) of 25–50%, or the need for renal replacement therapy. It is now recognized that changes in GFR are delayed manifestations of renal injury, and the development of urinary biomarkers may help to identify AKI earlier in the course of injury. The major causes of AKI in hospitalized patients include prerenal causes (~40%), postrenal causes (~5–10%), and intrinsic diseases affecting blood vessels, glomeruli, or tubules. Of the intrinsic causes, tubular disorders (acute tubular necrosis and acute interstitial nephritis) are the most common etiologies, accounting for 40–50% of all causes of AKI. Acute glomerulonephritis and vascular disorders are rare etiologies of AKI in hospitalized patients (〈5%).

scholarly journals Rifampicin Induced Acute Interstitial Nephritis in a Patient with Tubercular Lymphadenitis: A Case Report

2018 ◽  
Vol 8 (3) ◽  
pp. 257-259
Author(s):  
Hafsa Hassan Khan ◽  
Muhammad Abdur Rahim ◽  
Mehruba Alam Ananna ◽  
Tufayel Ahmed Chowdhury ◽  
Sarwar Iqbal
Keyword(s):  
Acute Kidney Injury ◽  
Case Report ◽  
Adverse Effects ◽  
Interstitial Nephritis ◽  
Case History ◽  
Kidney Injury ◽  
Acute Interstitial Nephritis ◽  
History Of ◽  
Tubercular Lymphadenitis ◽  
Prompt Diagnosis

Rifampicin is one of the most effective anti-tubercular agents. Among its rare adverse effects, acute interstitial nephritis (AIN) is noteworthy. Here, we describe the case history of a 55-year-old female with tubercular lymphadenitis who developed rifampicin induced AIN upon re-exposure and recovered satisfactorily without requiring steroids. Rifampicin induced AIN should be kept in mind when patients present with acute kidney injury as prompt diagnosis and discontinuation of the drug has excellent prognosis.Birdem Med J 2018; 8(3): 257-259

scholarly journals Time to Acute Kidney Injury in β-Lactam−Induced Acute Interstitial Nephritis

2020 ◽  
Vol 5 (7) ◽  
pp. 1068-1070 ◽  
Author(s):  
Benjamin Lazarus ◽  
Matthew R.P. Davies ◽  
Jason A. Trubiano ◽  
Rebecca Pellicano
Keyword(s):  
Acute Kidney Injury ◽  
Interstitial Nephritis ◽  
Kidney Injury ◽  
Acute Interstitial Nephritis

scholarly journals SP222The long term renal outcome in patients with biopsy proven acute tubular necrosis and acute interstitial nephritis

2019 ◽  
Vol 34 (Supplement_1) ◽  
Author(s):  
Cho Won-Yong ◽  
Jun Yong Lee ◽  
Kim Hyunseo ◽  
Ki Joon Lim ◽  
Yang Jihyun ◽  
...  
Keyword(s):  
Interstitial Nephritis ◽  
Acute Tubular Necrosis ◽  
Acute Interstitial Nephritis ◽  
Renal Outcome ◽  
Tubular Necrosis

Continuous Peritoneal Dialysis Compared with Daily Hemodialysis in Patients with Acute Kidney Injury

2009 ◽  
Vol 29 (2_suppl) ◽  
pp. 62-71 ◽  
Author(s):  
Daniela Ponce Gabriel ◽  
Jacqueline Teixeira Caramori ◽  
Luis Cuadrado Martin ◽  
Pasqual Barretti ◽  
Andre Luis Balbi
Keyword(s):  
Acute Kidney Injury ◽  
Renal Function ◽  
Peritoneal Dialysis ◽  
Survival Rate ◽  
Acute Tubular Necrosis ◽  
Kidney Injury ◽  
Acid Base ◽  
Tubular Necrosis ◽  
Daily Hemodialysis ◽  
Continuous Peritoneal Dialysis

Background In some parts of the world, peritoneal dialysis is widely used for renal replacement therapy (RRT) in acute kidney injury (AKI), despite concerns about its inadequacy. It has been replaced in recent years by hemodialysis and, most recently, by continuous venovenous therapies. We performed a prospective study to determine the effect of continuous peritoneal dialysis (CPD), as compared with daily hemodialysis (dHD), on survival among patients with AKI. Methods A total of 120 patients with acute tubular necrosis (ATN) were assigned to receive CPD or dHD in a tertiary-care university hospital. The primary endpoint was hospital survival rate; renal function recovery and metabolic, acid–base, and fluid controls were secondary endpoints. Results Of the 120 patients, 60 were treated with CPD (G1) and 60 with dHD (G2). The two groups were similar at the start of RRT with respect to age (64.2 ± 19.8 years vs 62.5 ± 21.2 years), sex (men: 72% vs 66%), sepsis (42% vs 47%), shock (61% vs 63%), severity of AKI [Acute Tubular Necrosis Individual Severity Score (ATNISS): 0.68 ± 0.2 vs 0.66 ± 0.22; Acute Physiology and Chronic Health Evaluation (APACHE) II: 26.9 ± 8.9 vs 24.1 ± 8.2], pre-dialysis blood urea nitrogen [BUN (116.4 ± 33.6 mg/dL vs 112.6 ± 36.8 mg/dL)], and creatinine (5.85 ± 1.9 mg/dL vs 5.95 ± 1.4 mg/dL). In G1, weekly delivered Kt/V was 3.59 ± 0.61, and in G2, it was 4.76 ± 0.65 ( p < 0.01). The two groups were similar in metabolic and acid–base control (after 4 sessions, BUN < 55 mg/dL: 46 ± 18.7 mg/dL vs 52 ± 18.2 mg/dL; pH: 7.41 vs 7.38; bicarbonate: 22.8 ± 8.9 mEq/L vs 22.2 ± 7.1 mEq/L). Duration of therapy was longer in G2 (5.5 days vs 7.5 days; p = 0.02). Despite the delivery of different dialysis methods and doses, the survival rate did not differ between the groups (58% in G1 vs 52% in G2), and recovery of renal function was similar (28% vs 26%). Conclusion High doses of CPD provided appropriate metabolic and pH control, with a rate of survival and recovery of renal function similar to that seen with dHD. Therefore, CPD can be considered an alternative to other forms of RRT in AKI.

When acute kidney injury in the intensive care unit is not acute tubular necrosis: A case report of κ-light chain crystalline tubulopathy

2019 ◽  
Vol 91 (5) ◽  
pp. 311-316
Author(s):  
Neal Shah ◽  
Ivy Rosales ◽  
Rex Neal Smith ◽  
Jacob E. Berchuck ◽  
Andrew J. Yee ◽  
...  
Keyword(s):  
Intensive Care Unit ◽  
Acute Kidney Injury ◽  
Intensive Care ◽  
Case Report ◽  
Light Chain ◽  
Acute Tubular Necrosis ◽  
Kidney Injury ◽  
Tubular Necrosis

scholarly journals Long-term Renal Outcome of Biopsy-proven Acute Tubular Necrosis and Acute Interstitial Nephritis

2020 ◽  
Vol 35 (26) ◽  
Author(s):  
Hyunseo Kim ◽  
Sang Kyung Jo ◽  
Shin Young Ahn ◽  
Young Joo Kwon ◽  
Hajeong Lee ◽  
...  
Keyword(s):  
Interstitial Nephritis ◽  
Acute Tubular Necrosis ◽  
Acute Interstitial Nephritis ◽  
Renal Outcome ◽  
Tubular Necrosis
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