Acute tubulointerstitial nephritis with uveitis syndrome presenting as multiple tubular dysfunction including Fanconi's syndrome

PURPOSE This study was performed to identify risk factors of ifosfamide-induced renal damage. PATIENTS AND METHODS Renal function was assessed in 120 patients at a minimum of 3 months after completion of chemotherapy including ifosfamide. The cumulative ifosfamide dose ranged from 2 to 95 g/m2 (median, 30 g/m2). Ten patients had undergone unilateral nephrectomy; combination cytostatic treatment included cisplatin in 51 and methotrexate in 57. Sixty-eight patients had received gentamicin treatment. The glomerular filtration rate was estimated using the Schwartz formula. Proximal tubular function was assessed by the percent reabsorptions of glucose and 16 amino acids, the fractional excretion of sodium, and the fractional reabsorption of phosphate. In addition, the serum bicarbonate level was measured. RESULTS Proximal tubular dysfunction--with a predominance of renal amino acid (66.3%) and phosphate loss (38.3%)--was much more frequent than both glomerular impairment and acidosis. Seven patients were identified as having renal Fanconi's syndrome, and generalized tubulopathy was noted in another 15 patients. Ifosfamide-induced nephrotoxicity was dose-dependent, with a weak linear inverse correlation between cumulative ifosfamide dose and fractional phosphate reabsorption. Unilateral nephrectomy proved to be the single most important risk factor (odds ratio for the development of renal Fanconi's syndrome, 11.4), but cisplatin also significantly enhanced ifosfamide-mediated nephrotoxicity. Methotrexate, gentamicin, and patient age at primary diagnosis had no influence on renal function. CONCLUSION Ifosfamide chemotherapy should probably be restricted in patients after unilateral nephrectomy.

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Tubulointerstitial nephritis and uveitis syndrome (TINU) with Fanconi’s syndrome

Clinical Nephrology ◽

10.5414/cn106471 ◽

2011 ◽

Cited By ~ 1

Author(s):

Y.-H. Yao ◽

C.-C. Lin ◽

Y.-M. Chung ◽

A.-H. Yang ◽

S.-Y. Li ◽

...

Keyword(s):

Tubulointerstitial Nephritis ◽

Fanconi’S Syndrome ◽

Fanconi's Syndrome

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Fanconi's syndrome and tubulointerstitial nephritis in association with L-lysine ingestion

American Journal of Kidney Diseases ◽

10.1016/s0272-6386(96)90476-x ◽

1996 ◽

Vol 28 (4) ◽

pp. 614-617 ◽

Cited By ~ 13

Author(s):

Joan C. Lo ◽

Glenn M. Chertow ◽

Helmut Rennke ◽

Julian L. Seifter

Keyword(s):

Tubulointerstitial Nephritis ◽

Fanconi’S Syndrome ◽

Fanconi's Syndrome

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Reversible tubular dysfunction that mimicked Fanconi's syndrome in a patient with anorexia nervosa

International Journal of Eating Disorders ◽

10.1002/eat.1078 ◽

2001 ◽

Vol 30 (2) ◽

pp. 227-230 ◽

Cited By ~ 10

Author(s):

George Alexandridis ◽

George Liamis ◽

Moses Elisaf

Keyword(s):

Anorexia Nervosa ◽

Tubular Dysfunction ◽

Fanconi’S Syndrome ◽

Fanconi's Syndrome

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Acute tubulointerstitial nephritis in children and chronic kidney disease

Archives de Pédiatrie ◽

10.1016/j.arcped.2019.05.002 ◽

2019 ◽

Vol 26 (5) ◽

pp. 290-294 ◽

Cited By ~ 3

Author(s):

S. Clavé ◽

C. Rousset-Rouvière ◽

L. Daniel ◽

M. Tsimaratos

Keyword(s):

Chronic Kidney Disease ◽

Kidney Disease ◽

Tubulointerstitial Nephritis ◽

Acute Tubulointerstitial Nephritis

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Urinary Cytokines Reflect Renal Inflammation in Acute Tubulointerstitial Nephritis: A Multiplex Bead-Based Assay Assessment

Journal of Clinical Medicine ◽

10.3390/jcm10132986 ◽

2021 ◽

Vol 10 (13) ◽

pp. 2986

Author(s):

Laura Martinez Valenzuela ◽

Juliana Draibe ◽

Oriol Bestard ◽

Xavier Fulladosa ◽

Francisco Gómez-Preciado ◽

...

Keyword(s):

Tubulointerstitial Nephritis ◽

Urinary Concentration ◽

Blood Eosinophil ◽

Acute Tubulointerstitial Nephritis ◽

Luminex Assay ◽

Non Invasive ◽

Urinary Levels ◽

Histological Data ◽

The Individual ◽

Multiplex Bead

Background: Acute tubulointerstitial nephritis (ATIN) diagnosis lays on histological assessment through a kidney biopsy, given the absence of accurate non-invasive biomarkers. The aim of this study was to evaluate the accuracy of different urinary inflammation-related cytokines for the diagnostic of ATIN and its distinction from acute tubular necrosis (ATN). Methods: We included 33 patients (ATIN (n = 21), ATN (n = 12)), and 6 healthy controls (HC). We determined the urinary levels of 10 inflammation-related cytokines using a multiplex bead-based Luminex assay at the time of biopsy and after therapy, and registered main clinical, analytical and histological data. Results: At the time of biopsy, urinary levels of I-TAC/CXCL11, CXCL10, IL-6, TNFα and MCP-1 were significantly higher in ATIN compared to HC. A positive correlation between the extent of the tubulointerstitial cellular infiltrates in kidney biopsies and the urinary concentration of I-TAC/CXCL11, MIG/CXCL9, CXCL10, IL17, IFNα, MCP1 and EGF was observed. Notably, I-TAC/CXCL11, IL-6 and MCP-1 were significantly higher in ATIN than in ATN, with I-TAC/CXCL11 as the best discriminative classifier AUC (0.77, 95% CI 0.57–0.95, p = 0.02). A combinatory model of these three urinary cytokines increased the accuracy in the distinction of ATIN/ATN compared to the individual biomarkers. The best model resulted when combining the three cytokines with blood eosinophil and urinary leukocyte counts (LR = 9.76). Follow-up samples from 11ATIN patients showed a significant decrease in I-TAC/CXCL11, MIG/CXCL9 and CXCL10 levels. Conclusions: Urinary I-TAC/CXCL11, CXCL10, IL6 and MCP-1 levels accurately distinguish patients developing ATIN from ATN and healthy individuals and may serve as novel non-invasive biomarkers in this disease.

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Cockayne syndrome with recurrent acute tubulointerstitial nephritis

Pathology International ◽

10.1111/j.1440-1827.2006.02029.x ◽

2006 ◽

Vol 56 (11) ◽

pp. 678-682 ◽

Cited By ~ 8

Author(s):

Satoshi Funaki ◽

Shori Takahashi ◽

Hitohiko Murakami ◽

Kensuke Harada ◽

Hiroshi Kitamura

Keyword(s):

Tubulointerstitial Nephritis ◽

Cockayne Syndrome ◽

Acute Tubulointerstitial Nephritis

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Acute Tubulointerstitial Nephritis in a Patient on Anti-Programmed Death-Ligand 1 Triggered by COVID-19: A Case Report

Canadian Journal of Kidney Health and Disease ◽

10.1177/20543581211014745 ◽

2021 ◽

Vol 8 ◽

pp. 205435812110147

Author(s):

Dimitry Buyansky ◽

Catherine Fallaha ◽

François Gougeon ◽

Marie-Noëlle Pépin ◽

Jean-François Cailhier ◽

...

Keyword(s):

Case Report ◽

Severe Acute Respiratory Syndrome ◽

Tubulointerstitial Nephritis ◽

Checkpoint Inhibitor ◽

Checkpoint Inhibitors ◽

High Dose ◽

Programmed Death Ligand 1 ◽

Acute Tubulointerstitial Nephritis ◽

Programmed Death ◽

Kidney Involvement

Rationale: Immune checkpoint inhibitors are monoclonal antibodies used in the treatment of various types of cancers. The downside of using such molecules is the potential risk of developing immune-related adverse events. Factors that trigger these autoimmune side effects are yet to be elucidated. Although any organ can potentially be affected, kidney involvement is usually rare. In this case report, we describe the first known instance of a patient being treated with an inhibitor of programmed death-ligand 1 (anti-PD-L1, a checkpoint inhibitor) who develops acute tubulointerstitial nephritis after contracting the severe acute respiratory syndrome coronavirus 2. Presenting concerns of the patient: A 62-year-old patient, on immunotherapy treatment for stage 4 squamous cell carcinoma, presents to the emergency department with symptoms of lower respiratory tract infection. Severe acute kidney injury is discovered with electrolyte imbalances requiring urgent dialysis initiation. Further testing reveals that the patient has contracted the severe acute respiratory syndrome coronavirus 2. Diagnosis: A kidney biopsy was performed and was compatible with acute tubulointerstitial nephritis. Interventions: The patient was treated with high dose corticosteroid therapy followed by progressive tapering. Outcomes: Rapid and sustained normalization of kidney function was achieved after completion of the steroid course. Novel findings: We hypothesize that the viral infection along with checkpoint inhibitor use has created a proinflammatory environment which led to a loss of self-tolerance to renal parenchyma. Viruses may play a more important role in the pathogenesis of autoimmunity in this patient population than was previously thought.

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