Tubulo-interstitial nephritis Flashcards
(30 cards)
What is TIN?
It involves inflammation & injury of the renal tubules & interstitial tissue, sparing the glomeruli initially
The tubulo-interstitial compartment plays a crucial role in?
π Fluid & electrolyte balance
π Hormone Secretion (e.g erythropoietin)
π Acid-base homeostasis
What is acute TIN?
Sudden onset with Inflammation and edema
What is Chronic TIN?
Gradual onset with fibrosis & irreversible damage
Acute TIN is more common in?
Hospitalized patients due to medication exposure (e.g antibiotics, NSAIDS)
Chronic TIN is more common in?
Populations with exposure to nephrotoxins or untreated metabolic disorders
The prevalence increases with age
What are the risk factors of TIN?
π Auto-immune diseases
π Prolonged drug use
π Recurrent urinary tract infections
What are the causes of ATIN?
π Drugs (NSAIDS, Antibiotics, Proton pump inhibitors)
π Infections (Bacterial- Strept, Leptospirosis)
(Viral- HIV,CMV,EBV)
π Systemic Diseases (Lupus nephritis, Sjorgenβs Syndrome)
π Idiopathic
What are the causes of CTIN?
π Drugs & Toxins (Long term use of lithium/heavy metalsβ lead & cadmium)
Herbal medicines
π Obstruction (Reflux nephropathy, Prolonged obstruction from stones or tumours)
π Metabolic disorders (Hypercalcemia & Gout-associated nephropathy)
π Chronic infections (Tb, fungal infections)
Explain the Pathophysiology of ATIN
It is an immune-mediated process which involves;
π Drug molecules which act as haptens & trigger a hypersensitivity reaction
πT-cell infiltration which leads to Tubulitis and interstitial edema
Explain the Pathophysiology of CTIN
Persistent inflammation & injury result in:
π Fibrosis & Tubular atrophy
π Loss of functional nephrons
What are the key mediators in TIN?
π Cytokines (IL-1, TNF-alpha)
π Growth factors (TGF-beta)
Clinical features of ATIN
π Fever, rash & eosinophilia (classic triad in drug-induced ATIN)
π Flank pain, oliguria or hematuria
Case example: A 40 year old patient on antibiotics presenting with AKI and generalized rash
Clinical features of CTIN
π Polyuria & Nocturia
π Fatigue, Nausea & Hypertension
What is the Classic triad seen in drug-induced ATIN?
Fever, rash & eosinophilia
What are the laboratory findings in TIN?
Urinalysis:
Pyuria, Mild Proteinuria (<1g/day), hematuria
Blood tests:
πElevated serum creatinine
πEosinophilia & Elevated inflammatory markers in ATIN
What is seen on ultrasound in diagnosis of TIN?
π ATINβ Enlarged Kidneys
π CTINβ Shrunken Kidneys
What is seen on CT Scan in diagnosis of TIN?
It may detect obstruction, calcifications or masses
What are the diagnostic imaging techniques used in TIN?
USS
CT
MRI
What are the indications for renal biopsy in TIN?
π Diagnostic uncertainty or suspected ATIN without clear etiology
π Monitoring for fibrosis in CTIN
What are the findings on renal biopsy in TIN?
π ATINβ Interstitial edema, Lymphocytic infiltrate, Tubular injury
π CTINβ Tubular atrophy, Interstitial fibrosis
What are the differentials of TIN?
Glomerulonephritis
Acute tubular necrosis
Pyelonephritis
GAP
What are the complications of TIN?
π Progression to CKD or ESRD in chronic cases.
π Persistent electrolyte abnormalities (e.g., hyperkalemia).
π Recurrent infections or secondary glomerular damage.
What is the management of TIN?
π Identify and address the underlying cause.
π Provide supportive care to enhance renal recovery.
