Brief explanation of each *refer harrison textbook for details causes of TIN Acute interstitial nephritis Chronic interstitial nephritis Reflux nephropathy Papillary necrosis Sickle-cell nephropathy

1. TUBULOINTER
STITIAL
NEPHRITISMARYAM JAMILAH BINTI ABDUL HAMID
082013100002
IMS BANGALORE

2. LEARNING OUTCOME
➤Acute interstitial nephritis
➤Chronic interstitial nephritis
➤Reflux nephropathy
➤Papillary necrosis
➤Sickle-cell nephropathy

5. INTRODUCTION
➤ affects renal tubules and interstitial components of the renal
parenchyma
➤ characterized: tubular dysfunction with electrolytes
abnormalities (moderate proteinuria, varying degrees of renal
impairment)

6. Acute
Interstitial Nephritis

7. DEFINITION
➤ characterized by acute inflammation affecting the tubulo-interstitium
of kidney, cellular and fluid exudation in the interstitial tissue
accompanied by but not dependent on degeneration of the
epithelium
➤ exudation not purulent, lesion can be diffuse and focal
➤ commonly caused by drug-induced, renal toxin, systemic diseases
and infection

8. ETIOLOGY
Immune
Allergic
Infections
Toxic
Autoimmune nephritis +-
uveitis, transplant
rejection
Penicillins, NSAIDS, PPI,
Mesalazine
Acute bacterial pyelonephritis,
Leptospirosis, Tuberculosis,
Hantavirus
Myeloma light chains,
mushroom (Cortinarius)

9. ●Nonsteroidal anti-inflammatory agents (NSAIDs), including selective
cyclooxygenase (COX)-2 inhibitors
●Penicillins and cephalosporins
●Rifampin
●Antimicrobial sulfonamides, including trimethoprim-sulfamethoxazole
●Diuretics, including loop diuretics such as furosemide and bumetanide, and
thiazide-type diuretics
●Ciprofloxacin and, perhaps to a lesser degree, other quinolones
●Cimetidine (only rare cases have been described with other H-2 blockers
such as ranitidine) [24,25]
●Allopurinol
●Proton pump inhibitors (PPIs) such as omeprazole and lansoprazole
●Indinavir
●5-aminosalicylates (eg, mesalamine)

10. PATHOGENESIS

11. CLINICAL FEATURES
➤ typically present as renal impairment
➤ drug-induced acute interstitial nephritis:
generalized drug hypersensitivity reaction,
fever, rash, eosinophilia.
➤ uveitis (5%); lymphocytes-predominant
interstitial nephritis. blurred vision, photophobia
➤ many patients not oliguric AKI

12. INVESTIGATION
➤ renal biopsy to confirm the diagnosis
intense inflammation, with infiltration of the tubules
and interstitium by polymorphonuclear leucocytes,
and lymphocytes
eosinophils maybe observed
degree of chronic inflammation in a biopsy is a
useful predictor of the eventual outcome for renal
function
➤ proteinuria (PCR <100 mg/mmol)
➤ urine; red & white blood cells but sterile culture

16. MANAGEMENT
➤withdrawal of the drug
➤high dose corticosteroids (prednisolone
1mg/kg/day) -accelerate recovery &
prevent long-term scarring
➤dialysis -short term

18. Chronic
Interstitial Nephritis

19. DEFINITION
➤characterized by renal dysfunction with fibrosis
and infiltration of the renal parenchyma by
lymphocytes, plasma cells and macrophages,
in association of tubular damage

20. ETIOLOGY
Glomerulo-
nephritis
Acute interstitial
nephritis
Immune/
Inflammatory
Toxic
varying of interstitial inflammation
occur in ass. most types of
inflammatory glomerulonephritis
Any cases of AIN if
persistent
sarcoidosis, Sjogren’s syndrome,
Chronic transplant rejection, SLE
Aristolochia in herbal medicines,
Lead, Balkan nephropathy,
Mushroom (Cortinarius)

21. Infection
Drugs
Congenital/
developmental
Metabolic &
systemic
diseases
Consequences of severe
polynephritis
All drugs causing AIN, tenofovir,
lithium toxicity, analgesic
nephropathy, ciclosporin,
tacrolimus
vesico-ureteric reflux, renal
dysplasias, inherited, Wilson’s
disease, medullary sponge kidney,
sickle cell nephropathy
calcium phosphate
crystallisation, hypokalemia,
hyperoxaluria
ETIOLOGY
(CONTINUE…)

23. CLINICAL FEATURES &
BIOCHEMICAL CHANGES➤adult life -CKD, hypertension, small kidneys
➤CKD stage 3 but tubular dysfunction, electrolyte
abnormalities are typically more severe,
resulting in hyperkalemia & acidosis.
➤minority; salt-losing nephropathy (hypotension,
polyuria, features of Na & H2O depletion)
➤impairment of urine-concentrating ability Na
conservation, risk of AKI due to salt & water
depletion during an acute illness

24. MANAGEMENT
➤supportive in nature, with correction
➤correction acidosis and hyperkalemia
➤replacement of fluid & electrolytes
➤RRT if irreversible renal damage

25. Reflux Nephropathy

26. DEFINITION
➤ previously known as chronic pyelonephritis
➤ specific type of chronic interstitial nephritis
➤ associated with vesico-ureteric reflux in early life
and appearance of scars in kidney, as
demonstrated by various imaging techniques

27. PATHOGENESIS
chronic reflux of urine from
bladder into ureters,, in
association with recurrent UTI in
childhood
*renal scars can happen without
infection
-VUR surgical correction ineffectively
halting the progress of disease
Genetic: VUR, renal dysplasia & other
renal congenital abnormalities of urinary
tract (outflow obstruction because of
urethral valves, but usually occur with an
apparent normal bladder

29. CLINICAL FEATURES
➤ asymptomatic (even with renal scarring and dilatation)
➤ proteinuria or features of CKD
➤ maybe no hx of overt UTI
➤ VUR in children but diminishes as the child grows
➤ risk renal stone increased
➤ women; proteinuria and/or hypertension in pregnancy
➤ small or unilateral renal scars have a good prognosis, provided
the renal growth is normal (compensatory hypertrophy of the
contralateral kidney)

30. INVESTIGATION
➤USG
➤MRI/CT scan assessing progression
➤gross scarring usually at poles with
reduced kidney size, narrowing of the
cortex and medulla (juxtaposed to
dilated calyces)
➤micturating cystourethrography

34. MANAGEMENT
➤ prophylactic UTI but no evidence protecting from
renal scarring or dysfunction
➤ recurrent pyelonephritis in abnormal kidney with
minimal function- nephrectomy
➤ no benefits on anti reflux surgery

35. Papillary Necrosis

36. Papillary Necrosis
➤ causes: DM, sickle-cell disease, longterm ingestion of
NSAID
➤ association with pyelonephritis but difficult to say it is
papillary necrosis or because of the complication of
pyelonephritis
➤ C/F: asymptomatic or renal colic & renal impairment
➤ urinalysis: normal/ hematuria & sterile pyuria. if proteinuria-
renal failure
➤ imaging: pyelography
➤ management: relieve the obstruction, withdrawal of the
offending drugs

37. Sickle-cell Nephropathy

38. Sickle-cell Nephropathy
➤Develop chronic complications of
microvascular occlusion
➤medulla most pronounced, vasa recta is site
of sickling because of hypoxia &
hypertonicity
➤C/F: loss urine concentrating ability
(polyuria), distal renal tubular acidosis,
impaired potassium excretion, papillary
necrosis can occur. *minority develop
ESRD

39. REFERENCES
➤ Davidson’s Principles and Practice of Medicine,
22nd Edition
➤ Harrison’s Internal Medicine, 19th Edition

40. Thank you….