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Tubulointerstitial Diseases of The Kidney

  1. Tubulointerstitial disease constitute a diverse group of acute and chronic hereditary and acquired disorders involving renal tubules and supporting structures.
  2. Functionally, they may result in nephrogenic diabetes insipidus with polyuria, nocturia, non – anion gap acidosis, salt wasting, and hypo or hyperkalemia. Azotemia is common. Proteinuria is modest.
  3. Because of polyuria and salt loosing nephropathy so hypertension is less common, and anemia may be severe. It is a type of salt loosing nephropathy.
Causes of Tubulointerstitial Disease (Ref. Hari. 18th ed., Pg - 2367, Table 285-1)
  1. Toxins
    1. Exogenous toxins
      1. Analgesic nephropathy
      2. Lead nephropathy
      3. Miscellaneous nephrotoxins (antibiotics, (beta lactam antibiotics) cyclosporine, radiographic contrast media, heavy metals)
    2. Metabolic toxins
      1. Acute uric acid nephropathy
      2. Gouty nephropathy
      3. Hypercalcemic nephropathy
      4. Hypokalemic nephropathy
      5. Miscellaneous (hyperoxaluria, cystinosis)
  2. Neoplasia
    1. Lymphoma
    2. Leukemia
    3. Multiple myeloma
  3. Immune disorders
    1. Hypersensitivity nephropathy
    2. Sjogren’s syndrome
    3. Amyloidosis
    4. Transplant rejection
    5. AIDS
  4. Vascular disorders
    1. Sickle cell nephropathy
  5. Hereditary renal diseases
    1. Hereditary nephritis (Alport’s syndrome)
  6. Infectious injury
    1. Acute pyelonephritis
    2. Chronic pyelonephritis
  7. Miscellaneous disorders
    1. Chronic urinary tract obstruction
    2. Vesicoureteral reflux
    3. Radiation nephritis.

Extra Edge

  1. Saturnine Gout is a type Tubulointerstitial Disease due to chronic lead poisoning. It is NOT due to uric acid. (FAQ) AIIMS May 10
  2. The fever of pyelonephritis typically exhibits a high, spiking "picket-fence" pattern and resolves over 72 h of therapy. Bacteremia develops in 20–30% of cases of pyelonephritis. (Ref. Hari. 18th ed., pg - 2390)
  3. Treatment strategies for acute uncomplicated cystitis (Ref. Hari. 18th ed., pg - 2393)
    1. Nitrofurantoin,
    2. TMP-SMX,
    3. Fosfomycin,
    4. Pivmecillinam,
    5. Fluoroquinolones,
    6. β-Lactams,


Important Points

Acute Interstitial Nephritis

  1. Drugs are a leading cause of Acute Interstitial Nephritis
  2. It presents with acute oliguria and sometimes fever, rash and arthralgias
  3. In addition to azotemia, tubular dysfunction may be present
  4. Eosinophilia is common. Urine analysis shows eosinophiluria. (AIPG 10) and/or WBC casts.
  5. On renal biopsy, interstitial edema with WBC infiltration is present.
  6. This disorder commonly responds to withdrawal of offending drug, and most patients have good recovery. Glucocorticoids may promote recovery.

Chronic Interstitial Nephritis
  1. Analgesic nephropathy is an important cause of this disorder and results from prolonged consumption of a combination of analgesics, usually of phenacetin and aspirin.
  2. Patients are often women with headaches, anemia, and GI symptoms.
  3. Manifestation includes uremia, acute papillary necrosis, sterile pyuria, or renal calculi.
  4. Renal function stabilizes with total cessation of drugs.
Functional Consequences of Tubulointerstitial Disease (Ref. Hari. 18th ed., pg - 1807, Table 279-2)
Defect Cause(s)
Fanconi syndrome Damage to proximal tubular reabsorption of glucose, amino acids, phosphate, and bicarbonate
Hyperchloremic acidosis 1. Reduced ammonia production
2. Inability to acidify the collecting duct fluid (distal renal tubular acidosis)
3. Proximal bicarbonate wasting
Tubular or small-molecular-weight proteinuria Failure of proximal tubule protein reabsorption
Polyuria, isosthenuria Damage to medullary tubules and vasculature
Hyperkalemia Potassium secretory defects including aldosterone resistance
Salt wasting Distal tubular damage with impaired sodium reabsorption
Reduced GFR (Late feature) Obliteration of microvasculature and obstruction of tubules

Treatment: Symptomatic
Renal papillary Necrosis
  1. Renal papillary necrosis is typically caused by ischaemic necrosis and sloughing of Renal Papillae
  2. It is clinically characterized by
    1. Loin Pain
    2. Hematuria
    3. Variable degree of renal impairment
Causes of papillary necrosis include:
  1. Diabetes (M/C cause)(LQ 2012)
  2. Sickle cell disease (LQ 2012)
  3. Analgesic Abuse Nephropathy
  4. Obstruction in association with infection
  5. Chronic alcoholism (LQ 2012)
  6. Vascular diseases

Extra Edge Tuberculosis is not a cause of necrotizing papillitis.


TABLE - Mechanisms for NSAID-Induced Disorders
NSAID-Induced Disorder Mechanism
1. Nephrotic syndrome Severe interstitial nephritis; histologically normal glomeruli
2. Decreased GFR Renal vasoconstriction, especially in patients with preexisting renal disease, congestive heart failure, or cirrhosis; patients treated with triamterene at particular risk
3. Papillary necrosis Unknown
4. Edema Primary renal sodium retention due to prostaglandin inhibition, especially in patients with underlying congestive heart failure
5. Hyperkalemia Hyporeninemic hypoaldosteronism

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