Renal Disease

Question 1

Tissue injury and clinical presentation in renal diseases

Answer 1

• Falling ability to filter/produce urine- accumulation of various waste products in blood, especially urea and creatinine; associated with acute renal failure
• Blood appearing in the urea- haematuria
• Protein loss into the urine- proteinuria
• Secondary problems, such as hypertension, anaemia etc.

Question 2

Acute tubular necrosis following hypoperfusion

Answer 2

• Tubular epithelial cells die
• Tubules dilate
• Sloughed epithelial cells lie in lumen-blocks the lumen, unable to produce urine
• Tubular function impaired
• Other components (glomeruli, vessels, interstium) preserved
• Renal function recovers (if patient survives)

Question 3

Acute tubular necrosis following hypoperfusion

Answer 3

• Tubular epithelial cells die
• Tubules dilate
• Sloughed epithelial cells lie in lumen-blocks the lumen, unable to produce urine
• Tubular function impaired
• Other components (glomeruli, vessels, interstium) preserved
• Renal function recovers (if patient survives)-epithelial cells regenerate
• The kidney is relatively protected against hypoxia
• Most common cause of acute renal failure

Question 4

Glomerulonephritis

Answer 4

• Acute injury to glomerulus, most often immune-mediated
• Mostly associated with deposition of immune complexes in the tuft- complement activation, formation of membrane attack complex etc
• Clinical consequences depend on what forms the complexes, where they lodge and how big they are
• Either acute and reversible, rapidly progressive (crescents) or slowly progressive-renal failure

Question 5

Glomerulonephritis without immune complexes

Answer 5

• Rare, but important
• Anti glomerular basement membrane disease
• Formation of specific anti-self antibodies directed against epitopes in our wo n glomerular basement membrane
• Light microscopy is the same as a florid, destructive immune complex mediated GN, often with crescents and acute renal failure

Question 6

Glomerulonephritis without immune complexes

Answer 6

• Rare, but important
• Anti glomerular basement membrane disease
• Formation of specific anti-self antibodies directed against epitopes in our own glomerular basement membrane
• Light microscopy is the same as a florid, destructive immune complex mediated GN, often with crescents and acute renal failure

Question 7

Pyelonephritis

Answer 7

• Bacterial infection of hte kidney affecting the parenchyma, calyces, renal pelvis
• Acute or chronic
• May occur with or without obstruction to urine flow
• Organisms ascend from the lower urinary tract to reach the kidney-septicaemia
• In adults, acute onset, fever, chills, ;umbar tenderness and pain, discomfort when urinating (frequently)
• Urine function usually preserved, hypertension not a component
• Urine containing organisms and WBCs
• In children, usually less clearly renal- abdominal pain, vomitting, fever
• Often gram negative bacteria

Question 8

Acute insterstitial nephritis

Answer 8

• Usually presents as acute renal failure-sometimes with some blood/ protein in urine
• Interstitium and tubules infiltrated by inflammatory cells, often with many eosinophils
• Often fever, maybe a rash
• Very often due to a drug allergy- or post streptococcal infection

Question 9

Non-immune deposits

Answer 9

Most common cause of renal failure is or will be diabetes mellitus.

• Glycosylated proteins
• Diabetic nephritis

Question 10

Genetic conditions- just know basically

Answer 10

• Polycystic kidney disease- gene on chromosome 16, cysts on liver, pancreas, small aneurysms in brains
• Alport syndrome- abnormality in collagen V- major component of the adult glomerular basement membrane. Haematuria, progressing deafness, ocular abnormalities, progression to end stage renal failure

Question 11

Effect of hypertension on kidneys

Answer 11

• Effects depend on pressure and duration

- End result- nephrosclerosis

Question 12

So-called ‘benign’ nephosclerosis

Answer 12

• Bilaterally shrunken granular kidneys
• Larger scars
• Histologically- atheroma of larger arteries, sclerosis of arteries, scarring of glomeruli and interstitium

Question 13

Future research in

Answer 13

• Genetic disorders
• Mechanisms of injury to the glomerular basement membrane in disorders of protein leakage
• Mechanisms of fibrosis in chronic renal injury (and dreams of stopping or reversing it)
• Arresting or reversing the damage caused by advanced glycation end products in diabetes mellitus
• etc. etc.