tubulointerstitial nephropathy

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^[1]^[2]^[3]

Introduction

Diseases of the renal tubules & interstitium.

Etiology

acute interstitial nephritis
secondary tubulointerstitial injury
immunologic (autoimmune disease)
infectious
- risk factors
  - pre-existing kidney disease
  - immunologic disease
- viral
  - polyoma BK virus (post renal transplantation)
  - JC virus
  - cytomegalovirus (CMV)
  - adenovirus
  - Epstein-Barr virus
  - hepatitis C virus
  - antiviral tenofovir used to treat HIV1, hepatitis B^[1]
- bacterial:
- Mycobacterial
  - Mycobacterium tuberculosis
  - Mycobacterium avium complex
- helminth infection: schistosomiasis
- mycosis (fungal infection)
- protozoan infection: toxoplasmosis
inherited
malignancy
pharmaceuticals
- analgesics (analgesic nephropathy)
  - phenacetin, aspirin, NSAIDs, COX2 inhibitors
- caffeine in combination with analgesics
- calcineurin inhibitors
  - cyclosporine, tacrolimus
- antivirals - tenofovir^[1]
- lithium carbonate
- proton pump inhibitors^[1]
- aristolochic acid nephropathy (Chinese herb)
  - Balkin endemic nephropathy
- prolonged exposure to any medication that can cause acute interstitial nephritis
  - allopurinol, cephalosporins, fluoroquinolones, H2 blockers, indinavir, mesalamine, penicillins, proton pump inhibitors, rifampin, sulfonamides
metabolic
obstructive uropathy
- prostatic hyperplasia
- urinary reflex nephropathy
- nephrolithiasis
- malignancies:

Pathology

antigens on tubular proteins or tubular epithelial cells may initiate renal injury
renal tubules, interstitium &/or genitourinay tract may be affected with relative sparing of the glomeruli
may result from renal glomerular disease (glomerulonephritis) or renal vascular disease
degree of tubulointerstitial fibrosis correlates with progression to end-stage renal disease
lymphocytic infiltration, interstitial fibrosis, renal tubular atrophy, arteriosclerosis, diffuse glomerulosclerosis

Genetics

autosomal dominant form
- family history of end-stage renal disease^[1]

Clinical manifestations

slowly progressive chronic renal failure
Fanconi syndrome
renal tubular acidosis
polyuria, isosthenuria, nocturia

Laboratory

complete blood count (CBC)
- anemia (injury to erythropoietin-producing cells)
- eosinophilia
serum chemistries
- serum urea nitrogen increased
- serum creatinine increased
- serum potassium: hyperkalemia
- serum bicarbonate decreased (RTA)
- serum phosphate low
glomerular filtration rate: decline in GFR
urine osmolality: isosthenuria
urine protein below nephrotic range (< 2 g/24 hours)
urinalysis
- pyuria, eosinophiluria
- occasional granular casts
- Fanconi syndrome
  - glucosuria despite normal serum glucose
  - aminoaciduria

Diagnostic procedures

renal ultrasound
- atrophic, echogenic kidneys consistent with chronic renal disease
- exclude obstructive uropathy
renal biopsy

Radiology

computed tomography as needed based upon renal ultrasound

Management

treatment generally results in limited improvement
treatment of underlying cause(s) may slow progression of disease
avoid nephrotoxic agents & use of intravenous contrast agents

More general terms

nephropathy

More specific terms

References

↑ ^1.0 ^1.1 ^1.2 ^1.3 ^1.4 Medical Knowledge Self Assessment Program (MKSAP) 15, 16, 17, 19 American College of Physicians, Philadelphia 2009, 2012, 2015, 2021
↑ Bleyer AJ, Hart PS, Kmoch S. Hereditary interstitial kidney disease. Semin Nephrol. 2010 Jul;30(4):366-73. Review. PMID: https://www.ncbi.nlm.nih.gov/pubmed/20807609 Free PMC Article
↑ Bollee G, Dahan K, Flamant M et al Phenotype and outcome in hereditary tubulointerstitial nephritis secondary to UMOD mutations. Clin J Am Soc Nephrol. 2011 Oct;6(10):2429-38. PMID: https://www.ncbi.nlm.nih.gov/pubmed/21868615 Free PMC Article

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