6 renal pathophysiology
TRANSCRIPT
Renal Pathology
Introduction:
• 150gm: each kidney
• 1700 liters of blood filtered 180 L of G. filtrate
1.5 L of urine / day.
• Kidney is a retro-peritoneal organ
• Blood supply: Renal Artery & Vein
• One half of kidney is sufficient – reserve
• kidney function: Filtration, Excretion, Secretion,
Hormone synthesis.
Kidney Location:
Kidney Anatomy:
Renal Pathology Outline
• Glomerular diseases: Glomerulonephritis
• Tubular diseases: Acute tubular necrosis
• interstitial diseases: Pyelonephritis
• Diseases involving blood vessels: Nephrosclerosis
• Cystic diseases
• Tumors
Clinical Syndromes:
• Nephritic syndrome.
– Oliguria, Haematuria, Proteinuria, Oedema.
• Nephrotic syndrome.
– Gross proteinuria, hyperlipidemia,
• Acute renal failure
– Oliguria, loss of Kidney function - within weeks
• Chronic renal failure.
– Over months and years - Uremia
Introduction
• Functions of the kidney:– excretion of waste products
– regulation of water/salt
– maintenance of acid/base balance
– secretion of hormones
• Diseases of the kidney– glomeruli
– tubules
– interstitium
– vessels
• Azotemia: BUN, creatinine
• Uremia: azotemia + more problems
• Acute renal failure: oliguria
• Chronic renal failure: prolonged uremia
Abnormal findings
• Hematuria
• Oliguria
• Azotemia
• Hypertension
Nephritic syndrome
• Massive proteinuria
• Hypoalbuminemia
• Edema
• Hyperlipidemia/-uria
Nephrotic syndrome
Glomerular diseases
– Nephrotic syndrome
• Minimal change disease
• Focal segmental glomerulosclerosis
• Membranous nephropathy
– Nephritic syndrome
• Post-infectious GN
• IgA (immune) nephropathy
Nephrotic Syndrome
• Massive proteinuria
• Hypoalbuminemia
• Edema
• Hyperlipidemia
• Adults: systemic disease (diabetes)
• Children: minimal change disease
• Characterized by loss of foot processes
• Good prognosis
Causes
Minimal change disease
Minimal change disease Normal glumerular structure
Normal glomerulusMinimal change disease
Focal Segmental Glomerulosclerosis
• Primary or secondary
• Some (focal) glomeruli show partial
(segmental) hyalinization
• Unknown pathogenesis
• Poor prognosis
Focal segmental glomerulosclerosis
Membranous Glomerulonephritis
• Autoimmune reaction against unknown renal antigen
• Immune complexes
• Thickened GBM
• Subepithelial deposits
Membranous glomerulonephritis
Nephritic Syndrome
• Hematuria
• Oliguria, azotemia
• Hypertension
• Post-infectious GN, IgA nephropathy
• Immunologically-mediated
• Characterized by proliferative changes and
inflammation
Causes
Post-Infectious Glomerulonephritis
• Child after streptococcal throat infection
• Immune complexes
• Hypercellular glomeruli
• Subepithelial humps
Post-infectious glomerulonephritis
IgA Nephropathy
• Common!
• Child with hematuria after (URI) Upper
Respiratory Infection
• IgA in mesangium
• Variable prognosis
IgA nephropathy
• Tubular and interstitial diseases
– Inflammatory lesions
• pyelonephritis
Pyelonephritis
• Invasive kidney infection
• Usually ascends from UTI
• Fever, flank pain
• Organisms: E. coli, Proteus
• Women, elderly
• Patients with catheters or mal-formations
• Dysuria, frequency
• Organisms: E. coli, Proteus
Urinary Tract Infection
Acute pyelonephritis with abscesses
Pyelonephritis
Cellular cast
Chronic pyelonephritis
Drug-Induced Interstitial Nephritis
• Antibiotics, NSAIDS
• IgE and T-cell-mediated immune reaction
• Fever, eosinophilia, hematuria
• Patient usually recovers
• Analgesic nephritis is different (bad)
Drug-induced interstitial nephritis
Acute Tubular Necrosis
• The most common cause of ARF!
• Reversible tubular injury
• Many causes: ischemic (shock), toxic (drugs)
• Most patients recover
Acute tubular necrosis
Benign Nephrosclerosis
• Found in patients with benign hypertension
• Hyaline thickening of arterial walls
• Leads to mild functional impairment
• Rarely fatal
Benign nephrosclerosis
Malignant nephrosclerosis
• Arises in malignant hypertension
• Hyperplastic vessels
• Ischemia of kidney
• Medical emergency
• 5% of cases of hypertension
• Super-high blood pressure, encephalopathy, heart
abnormalities
• First sign often headache, scotomas
• Decreased blood flow to kidney leads to increased
renin, which leads to increased BP!
• 5y survival: 50%
Malignant Hypertension
Malignant hypertension
Adult Polycystic Kidney Disease
• Autosomal dominant
• Huge kidneys full of cysts
• Usually no symptoms until 30 years
• Associated with brain aneurysms.
Adult polycystic kidney disease
Childhood Polycystic Kidney Disease
• Autosomal recessive
• Numerous small cortical cysts
• Associated with liver cysts
• Patients often die in infancy
Childhood polycystic kidney disease
Medullary Cystic Kidney Disease
• Chronic renal failure in children
• Complex inheritance
• Kidneys contracted, with many cysts
• Progresses to end-stage renal disease
• Tumors
– Renal cell carcinoma
– Bladder carcinoma
Renal Cell Carcinoma
• Derived from tubular epithelium
• Smoking, hypertension, cadmium exposure
• Hematuria, abdominal mass, flank pain
• If metastatic, 5y survival = 5%
Renal cell carcinoma
Bladder Carcinoma
• Derived from transitional epithelium
• Present with painless hematuria
• Prognosis depends on grade and depth of invasion
• Overall 5y survival = 50%
Bladder carcinoma