CLINICAL PRESENTATION OF

TUBULOINTERSTITIAL NEPHRITIS
Prof Dr Sevgi Şahin
 Tubulointerstitial nephritis

• Kidney diseases that involve structures in the

kidney outside the glomerulus.
• These diseases generally involve tubules and/or
the interstitium of the kidney and spare the
glomeruli.
 Pathophysiology

• Lethal, sublethal injury to renal cells lead to

expression of new local antigens, inflammatory cell
infiltration and activation of proinflammatory cells
and cytokines
• Acute- renal tubular dysfunction with or without
renal failure ( If the tubular basement mebrane is
preserved- reversibile)
• Chronic- interstitial scarring fibrosis, tubule atrophy-
resulting progressive renal failure
 Acute interstitial nephritis

• The tubular damage leads to renal tubular dysfunction,

with or without renal failure.
• The renal dysfunction is generally reversible
• Drug induced ATIN is not dose dependent
• Fever, skin rash and eosinophilia in a minority of cases
• Mild proteinuria, hematuria and sterile pyuria,
eosinophiluria detected by Hansel’s stain
• Tubular dysfunction manifested as glycosuria,
aminoaciduria, potassium wasting, magnesium wasting
• Late manifestations: hypertension and anemia
Causes of acute tubulointerstitial nephritis

• Hypersensitivity reactions
• Immunologic diseases
• Infection related
Causes of acute tubulointerstitial nephritis
 Laboratory Findings

• Elevation in BUN, creatinine

• Urinalysis shows a predominance of WBCs and
WBC casts, eosinophiluria detected by Hansel’s
stain
• Mild proteinuria,
• Tubular dysfunction manifested as glycosuria,
aminoaciduria, potassium wasting, magnesium
wasting
• Late manifestations: hypertension and anemia
 Special Tests

• Ultrasound: non-sp findings (normal or slightly

enlarged kidney sizes, a mild degree of
increased echogenicity in ATIN)
• Gallium scanning: can distinguish ATIN from
ATN (ATIN: positive diffuse uptake)
 Tubulointerstitial Diseases

Definitive diagnosis by kidney biopsy

– Diagnosis often made clinically
– Biopsy may not alter therapy
Causes of Chronic Tubulointerstitial Nephritis
 Chronic Tubulointerstitial Nephritis

• There may be concomittant glomerular

abnormalities, probably secondary to maladaptive
alterations in the glomeruli or a result of the
tubulointerstitial processes
 Clinical presentation
Chronic
• Insidious nature
• Often diagnosed incidentally on routine laboratory
screening, or evaluation of hypertension
• Modest proteinuria, sterile pyuria, anemia, renal
insuff ( NSAID)
• Polyuria concentration defect (lithium)
• Modest proteinuria, hyperK renal tub. acidosis in chr.
obstruction
• Arterioscler. kidney: modest proteinuria, kreatinin
and BUN elevation, hypertension
 Laboratory

• BUN , creatinine- renal failure

• Low bicarbonate < 24 mEq L- acidosis ph<7,35
With hypoK – proximal tub. disorder
With hyperK- distal tub disoreder
• Urinalysis: hematuria and pyuria with-or without
bacteria, casts, eosinophils, crystals
• Urine protein usually <1-2 gr/24h
 Imaging

US/ and flat plate kidney- hydronephrosis, renal calculi

• Normal kidney size favours acute
• Small kidneys with increased echogenicity- chronic
disease

CT(high resolutional) scan show microcalcifications in

renal papillary tips- diagnosing analgesic
nephropathy
 Prognosis

• Most patients with allergic interstitial nephritis recover renal

function upon cessation of the offending agent.
• Tubulointerstitial disease may progress to end-stage renal disease
(ESRD) and thus require dialysis or transplantation.
• Electrolyte and acid-base disorders may also be observed
• Most chronic tubulointerstitial renal disease progresses to ESRD.
The rate of progression is much slower in tubulointerstitial
nephritis compared to glomerular diseases.