6 renal pathophysiology

57
Renal Pathology

Upload: shwetha-sulochana

Post on 16-Aug-2015

54 views

Category:

Documents


3 download

TRANSCRIPT

Page 1: 6  renal pathophysiology

Renal Pathology

Page 2: 6  renal pathophysiology

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.

Page 3: 6  renal pathophysiology

Kidney Location:

Page 4: 6  renal pathophysiology

Kidney Anatomy:

Page 5: 6  renal pathophysiology

Renal Pathology Outline

• Glomerular diseases: Glomerulonephritis

• Tubular diseases: Acute tubular necrosis

• interstitial diseases: Pyelonephritis

• Diseases involving blood vessels: Nephrosclerosis

• Cystic diseases

• Tumors

Page 6: 6  renal pathophysiology

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

Page 7: 6  renal pathophysiology

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

Page 8: 6  renal pathophysiology
Page 9: 6  renal pathophysiology

• Azotemia: BUN, creatinine

• Uremia: azotemia + more problems

• Acute renal failure: oliguria

• Chronic renal failure: prolonged uremia

Abnormal findings

Page 10: 6  renal pathophysiology

• Hematuria

• Oliguria

• Azotemia

• Hypertension

Nephritic syndrome

• Massive proteinuria

• Hypoalbuminemia

• Edema

• Hyperlipidemia/-uria

Nephrotic syndrome

Page 11: 6  renal pathophysiology
Page 12: 6  renal pathophysiology
Page 13: 6  renal pathophysiology
Page 14: 6  renal pathophysiology

Glomerular diseases

– Nephrotic syndrome

• Minimal change disease

• Focal segmental glomerulosclerosis

• Membranous nephropathy

– Nephritic syndrome

• Post-infectious GN

• IgA (immune) nephropathy

Page 15: 6  renal pathophysiology

Nephrotic Syndrome

• Massive proteinuria

• Hypoalbuminemia

• Edema

• Hyperlipidemia

Page 16: 6  renal pathophysiology

• Adults: systemic disease (diabetes)

• Children: minimal change disease

• Characterized by loss of foot processes

• Good prognosis

Causes

Page 17: 6  renal pathophysiology

Minimal change disease

Page 18: 6  renal pathophysiology

Minimal change disease Normal glumerular structure

Page 19: 6  renal pathophysiology

Normal glomerulusMinimal change disease

Page 20: 6  renal pathophysiology

Focal Segmental Glomerulosclerosis

• Primary or secondary

• Some (focal) glomeruli show partial

(segmental) hyalinization

• Unknown pathogenesis

• Poor prognosis

Page 21: 6  renal pathophysiology

Focal segmental glomerulosclerosis

Page 22: 6  renal pathophysiology

Membranous Glomerulonephritis

• Autoimmune reaction against unknown renal antigen

• Immune complexes

• Thickened GBM

• Subepithelial deposits

Page 23: 6  renal pathophysiology

Membranous glomerulonephritis

Page 24: 6  renal pathophysiology

Nephritic Syndrome

• Hematuria

• Oliguria, azotemia

• Hypertension

Page 25: 6  renal pathophysiology

• Post-infectious GN, IgA nephropathy

• Immunologically-mediated

• Characterized by proliferative changes and

inflammation

Causes

Page 26: 6  renal pathophysiology

Post-Infectious Glomerulonephritis

• Child after streptococcal throat infection

• Immune complexes

• Hypercellular glomeruli

• Subepithelial humps

Page 27: 6  renal pathophysiology

Post-infectious glomerulonephritis

Page 28: 6  renal pathophysiology

IgA Nephropathy

• Common!

• Child with hematuria after (URI) Upper

Respiratory Infection

• IgA in mesangium

• Variable prognosis

Page 29: 6  renal pathophysiology

IgA nephropathy

Page 30: 6  renal pathophysiology

• Tubular and interstitial diseases

– Inflammatory lesions

• pyelonephritis

Page 31: 6  renal pathophysiology

Pyelonephritis

• Invasive kidney infection

• Usually ascends from UTI

• Fever, flank pain

• Organisms: E. coli, Proteus

Page 32: 6  renal pathophysiology

• Women, elderly

• Patients with catheters or mal-formations

• Dysuria, frequency

• Organisms: E. coli, Proteus

Urinary Tract Infection

Page 33: 6  renal pathophysiology

Acute pyelonephritis with abscesses

Page 34: 6  renal pathophysiology

Pyelonephritis

Page 35: 6  renal pathophysiology

Cellular cast

Page 36: 6  renal pathophysiology
Page 37: 6  renal pathophysiology

Chronic pyelonephritis

Page 38: 6  renal pathophysiology

Drug-Induced Interstitial Nephritis

• Antibiotics, NSAIDS

• IgE and T-cell-mediated immune reaction

• Fever, eosinophilia, hematuria

• Patient usually recovers

• Analgesic nephritis is different (bad)

Page 39: 6  renal pathophysiology

Drug-induced interstitial nephritis

Page 40: 6  renal pathophysiology

Acute Tubular Necrosis

• The most common cause of ARF!

• Reversible tubular injury

• Many causes: ischemic (shock), toxic (drugs)

• Most patients recover

Page 41: 6  renal pathophysiology

Acute tubular necrosis

Page 42: 6  renal pathophysiology

Benign Nephrosclerosis

• Found in patients with benign hypertension

• Hyaline thickening of arterial walls

• Leads to mild functional impairment

• Rarely fatal

Page 43: 6  renal pathophysiology

Benign nephrosclerosis

Page 44: 6  renal pathophysiology

Malignant nephrosclerosis

• Arises in malignant hypertension

• Hyperplastic vessels

• Ischemia of kidney

• Medical emergency

Page 45: 6  renal pathophysiology

• 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

Page 46: 6  renal pathophysiology

Malignant hypertension

Page 47: 6  renal pathophysiology

Adult Polycystic Kidney Disease

• Autosomal dominant

• Huge kidneys full of cysts

• Usually no symptoms until 30 years

• Associated with brain aneurysms.

Page 48: 6  renal pathophysiology

Adult polycystic kidney disease

Page 49: 6  renal pathophysiology

Childhood Polycystic Kidney Disease

• Autosomal recessive

• Numerous small cortical cysts

• Associated with liver cysts

• Patients often die in infancy

Page 50: 6  renal pathophysiology

Childhood polycystic kidney disease

Page 51: 6  renal pathophysiology

Medullary Cystic Kidney Disease

• Chronic renal failure in children

• Complex inheritance

• Kidneys contracted, with many cysts

• Progresses to end-stage renal disease

Page 52: 6  renal pathophysiology

• Tumors

– Renal cell carcinoma

– Bladder carcinoma

Page 53: 6  renal pathophysiology

Renal Cell Carcinoma

• Derived from tubular epithelium

• Smoking, hypertension, cadmium exposure

• Hematuria, abdominal mass, flank pain

• If metastatic, 5y survival = 5%

Page 54: 6  renal pathophysiology

Renal cell carcinoma

Page 55: 6  renal pathophysiology

Bladder Carcinoma

• Derived from transitional epithelium

• Present with painless hematuria

• Prognosis depends on grade and depth of invasion

• Overall 5y survival = 50%

Page 56: 6  renal pathophysiology
Page 57: 6  renal pathophysiology

Bladder carcinoma