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CPR96 Diseases of kidney II(Tubulointerstitial dis


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Tubulointerstitial disease types
1.Acute tubular injury (ischaemic or toxic injury) 2. Tubulointerstitial nephritis (inflammatory reactions of tubules and interstitium)
Acute tubular injury
Also known as acute tubular necrosis (ATN), Present as Acute Renal Failure
Acute tubular injury causes
Ischaemia, Direct toxic injury, Acute tubulointerstitial nephritis or Urinary obstruction (ischemia far more common than toxic injury)
Acute tubular injury by ischemia
↓or interrupted blood flow: Decreased effective circulating blood volume e.g. shock (pre-renal cause), Diffuse involvement of intrarenal blood vessels e.g malignant hypertension OR Thrombosis e.g. thrombotic microangiopathy
Acute tubular injury by direct toxic injury
e.g. drugs, radiocontrast dyes, myoglobin, heavy metals, organic solvents
Acute tubular injury by urinary obstruction
by prostatic hypertrophy or tumour or blood clot (post renal cause)
Acute tubular injury histology
Necrotic tubular epithelium sloughed in tubules, Dilated tubules with
Acute tubular injury 3 stages
Initiation phase (lasting for about 36 hours) -> Maintenance phase -> Recovery phase
Initiation phase
Slight decline in urine output with rise in blood urea and creatinine
Maintenance phase
↓ in urine output 40-400 mL/day (oliguria), salt and water overload, rising blood urea and creatinine, hyperkalemia (high blood potassium level), metabolic acidosis
Recovery phase
Steady increase in urine volume, up to 3L/day, leading to loss of large amount of water, sodium and potassium
Acute tubular injury outcome
With supportive care, most patients can recover; unless there are other conditions like sepsis, extensive burns and multi organ failure
Tubulointerstitial nephritis
Inflammatory injuries of the tubules AND interstitium, Glomeruli are SPARED
Acute tubulointerstitial nephritis
Usually presented as acute or subacute worsening of renal function (↑ urea and creatinine level), Usually 2 weeks after drug exposure
Tubulointerstitial nephritis causes
DRUGS, Infection (Acute and Chronic pyelonephritis), metabolic disease, neoplasm (Multiple myeloma -> light chain cast nephropathy), physical factors (chronic UT obstruction), Immunologic reaction (Sarcoidosis, Sjogren’s disease)
Tubulointerstitial nephritis by Metabolic disease
Urate nephropathy, nephrocalcinosis , acute phosphate nephropathy, hypokalaemic nephropathy, oxalate nephropathy
Tubulointerstitial nephritis Causative drugs
Basically all drug classes e.g. NSAIDs, Antibiotics, Diuretics, Antivirals, Anti-convulsant, Anti-depressants, Radiology contrast, Herbal remedies -> Most common form is hypersensitivity reaction to medications
Tubulointerstitial nephritis histology
Interstitial inflammation (Abundant eosinophils points to drug cause), Tubulitis (Inflammatory cells in between tubular cells), Interstitial edema (acute) or fibrosis (chronic)
Infection in kidney (Pyelonephritis)
Predominantly affects tubules, interstitium and renal pelvis
Pyelonephritis 2 major forms
Acute pyelonephritis/ Chronic pyelonephritis
Acute pyelonephritis
Acute infection of kidney, generally caused by bacteria
Chronic pyelonephritis
Scarred kidney caused by repeated bacterial infections
Acute pyelonephritis route
Ascending route/ Hematogenous route (Ascending bacterial infections are most common)
Acute pyelonephritis Predisposing causes
Lower urinary tract infection, urinary tract obstruction (stones/ tumour), Vesico-ureteric reflux, pregnancy, Instrumentation / catheterization of urinary tract, Immunosuppression and deficiency
Acute Pyelonephritis symptoms
High fever, Shaking chills, Loin pain, Nausea, Vomiting, Diarrhoea, Failure to thrive(in children)
Acute Pyelonephritis pathogens
Fungal/ Bacteria: E. coli, Proteus, Klebsiella, Enterobacter, Strept. Faecalis, Staphylococcus, MTB
Acute Pyelonephritis histology
Large amount of neutrophils in the interstitium & tubules, pus in medulla in gross organ
Acute Pyelonephritis Rx
appropriate antibiotic therapy -> Symptoms usually disappear in a few days & Usually COMPLETE resolution without leaving significant effects on kidney
Acute Pyelonephritis healing process
Neutrophilic infiltrates replaced by macrophages, plasma cells and lymphocytes & Scattered scar formation
Acute Pyelonephritis complications
Pyelonephrosis (Pus in renal pelvis, calyces and ureter), Perinephric abscess (Extension of pus through renal capsule into perinephric tissue)
Chronic Pyelonephritis
Chronic inflammation in tubules and interstitium (TB excluded), Scarred kidney caused by repeated bacterial infections & Involvement usually unequal on the two sides
Chronic Pyelonephritis association
Vesico-ureteric reflux/ Urinary tract obstruction (stone, stricture)
Chronic Pyelonephritis presentation
Recurrent acute pyelonephritis (high fever, shaking chills, loin pain), CKD & ESRD (Uremia)
Chronic Pyelonephritis caution
Can have subtle or no symptoms in early stage (polyuria and nocturia due to loss of tubular function in concentrating urine and resorption of water)
Chronic pyelonephritis histology (not Dx)
Tubulointerstitial injury (Tubular damage, Interstitial fibrosis and inflammation) -> In long term, glomerulus are also affected
Chronic pyelonephritis histology (glomeruli)
↓ functional glomeruli , Compensatory hypertrophy by remaining glomeruli, Progressive fibrosis involving portions of some glomeruli (FSGS) due to compensatory action, Further decrease in number of functional glomeruli and vicious cycle
Chronic pyelonephritis Rx
Treat possible underlying causes & Treat recurrent acute pyelonephritis by antibiotic therapy
Chronic pyelonephritis outcome
Depends on extent of scarring, If loss of significant amount of renal tissue -> ESRD
Light chain cast nephropathy
Neoplasm of plasma cells, also known as myeloma kidney (obsolete)
Light chain cast nephropathy epidemiology
Occurs in 30 50% patients with multiple myeloma, 90% of cases greater than age of 50 years old (median age 70 years old)
Light chain cast nephropathy presentation
Acute renal failure and proteinuria
Other renal diseases associated with monoclonal light chains
Amyloidosis (AL type), Light chain deposition disease, Light chain proximal tubulopathy, Type I Cryoglobulinemic glomerulonephritis
Light chain cast nephropathy Rx
Treat underlying plasma cell neoplasm, Hematopoietic stem cell transplantation in selected case
Light chain cast nephropathy Prognosis
5 year survival rate: 20-25%
Vascular disease example
Hypertensive nephrosclerosis, Malignant nephrosclerosis (malignant HT), DM nephropathy (Affecting both vessels and glomeruli), ANCA associated vasculitis, Thrombotic microangiopathy (Haemolytic uraemic syndrome, Atypical haemolytic uraemic syndrome, Thrombotic thrombocytopenic purpura), Renal artery stenosis, Atheroemboli
Hypertensive nephrosclerosis
Strongly associated with hypertension, Sclerosis of renal arterioles and small arteries
Hypertensive nephrosclerosis changes
Hyalinization of arteriolar wall (Extravasation of plasma protein through injured endothelium) & Intimal fibrosis and medial thickening
Hypertensive nephrosclerosis pathogenesis
Affected vessels (thickened walls and narrowed lumens) -> ischaemia and subsequent glomerulosclerosis and chronic tubulointerstitial injury -> gradual decline in renal function -> chronic renal failure --> ESRD
Hypertensive nephrosclerosis histology
Intimal fibrosis and medial thickening of artery, Glomerulosclerosis and
Malignant nephrosclerosis
Associated with malignant or accelerated hypertension (SBP > 200 mmHg AND/OR DBP > 120)
Malignant nephrosclerosis presentation
Acute renal failure with Papilloedema , retinal haemorrhages, encephalopathy, CV abnormalities
Malignant nephrosclerosis histology
Fibrinoid necrosis of arteriole & Hyperplastic arteriolitis (onion skin lesion)
Malignant nephrosclerosis Rx
Prompt and aggressive antihypertensive medication
Diabetic nephropathy etiology
Both Type I and Type II Diabetes mellitus (DM)
Diabetic nephropathy
Renal vascular lesions, in the form of arteriolosclerosis, also affect glomeruli (thicken GBM, Diffuse increase in mesangial matrix, Kimmeltiel-Wilson nodules)
Diabetic nephropathy pathogenesis
Leading to ischaemia and subsequent glomerulosclerosis and chronic tubulointerstitial injury -> Eventually gradual decline in renal function --> chronic renal failure --> ESRD
Diabetic nephropathy histology
Hyalinosis of both afferent and efferent arterioles, Increase in mesangial matrix, Kimmelstiel Wilson nodules, GBM thickened to more than 1000 nm (arrowed)
ANCA-associated vasculitis
One of the causes of rapidly progressive (crescentic) glomerulonephritis (Type III, Pauci immune)
ANCA-associated vasculitis Ix problem
Lack of detectable anti GBM antibodies or immune complex by direct immunofluorescence and electron microscopy --> Pauci immune
ANCA-associated vasculitis Ix
Usually have circulating antineutrophil cytoplasmic antibodies (ANCAs) in blood: c-ANCA (cytoplasmic) & p-ANCA (perinuclear)
ANCA-associated vasculitis Disease entity
Wegener granulomatosis (granulomatosis with polyangiitis) & Microscopic polyangiitis
ANCA-associated vasculitis histology
Destruction of GBM, Crescent formation & Destroyed blood vessel wall with fibrin deposition, Negative study for direct immunofluorescence and electron microscopy