RENAL REVISION QUIZ

What are the three layers of the glomerular filter?

Endothelium negatively charged endothelial cells

Basement membrane type IV collagen, laminin, fibronectin, negatively charged proteoglycans

Podocyte/pedicels negatively charged

What is the Cockcroft-Gault equation

Estimated GFR (mL/min) =(140-age) * weight (kg)180 * plasma [creatinine]

Multiple this by 0.85 for women

How does noradrenaline affect GFR?

1. Dilates the afferent arteriole, leading to decreased GFR

2. Constricts the afferent arteriole, leading to increased GFR

3. Constricts the efferent arteriole, leading to increased GFR

4. Constricts the afferent arteriole leading to decreased GFR

How does angiotensin affect GFR?

1. Dilates the afferent arteriole, leading to decreased GFR

2. Constricts the afferent arteriole, leading to increased GFR

3. Constricts the efferent arteriole, leading to increased GFR

4. Constricts the afferent arteriole leading to decreased GFR

Let’s draw a nephron and show what gets

secreted/absorbed along its length!!

What 3 mechanisms does the kidney use to regulate pH?

H+ secretion upregulated by aldosterone; occurs in intercalated cells

HCO3- reabsorption mostly in proximal tubules; also thick ascending LoH and early distal tubules

Buffers phosphate buffer system and ammonia buffer system

Define acute renal failure >50% decrease in GFR in hours/days Can also have increased BUN Can also have decreased urine output

Which is NOT a consequence of ARF?

1. Hypokalaemia2. Oedema3. Hypertension4. Anaemia

Define CKD? GFR < 60mL/min/1.73m2 for > 3 months

with or without evidence of kidney damage

OR Evidence of kidney damage with or

without decreased GFR for > 3 months

If someone is in stage 3 CKD, what management must you

implement? Cardiovascular risk reduction lifestyle,

BP, lipid-lowering, diabetic control Monitor eGFR every 3 months Avoid nephrotoxic drugs Prescribe ACEI

Name some complications of diabetes

Retinopathy Nephropathy Neuropathy MI Stroke Gangrene infection

What three factors contribute to diabetic glomerular sclerosis

Metabolic defect; insulin deficiency hyperglycaemia biochemical alterations in GBM (increased collagen type IV and fibronectin, decreased proteoglycan) and increased ROS ( damage)

Nonenzymatic glycosylation inflammatory cytokines and GF released from macrophages, ROs generation in endothelial cells, increased procoagulant activity in endothelial cells and macrophages, ECM synthesis and SM prolif.

Haemodynamic changes increased GFR, glomerular capillary pressure, glomerular filtration area, and glomerular hypertrophy. Afferent arteriole is damaged bigger afferent than efferent

increased GFR and pressure, causing further damage and increased shearing forces mesangial cell hypertrophy and excretion of ECM products glomerular sclerosis

Which type of dialysis uses a hydrostatic gradient?

Peritoneal dialysis Hemodialysis

Peritoneal dialysis uses an osmotic gradient

A patient presents with intermittent haematuria, flank pain and a palpable mass. He

complains of malaise and fever. He is a heavy smoker, obese and

has hypertension. What investigations would you order?

Urinalysis: haematuria Blood: electrolytes, creatinine, BUN Paraneoplastic syndromes: FBC, ESR, LFTs, serum

calcium LDH (prognosis) Renal U/S or abdominal CT cystic Vs solid CXR lung metastases

What are the conditions of refusing life-sustaining

measures One of

Incurable/irreversible terminal illness, expected to die within a year

Persistent vegetative state Permenantly unconscious No reasonable prospect of recovery without life-

sustaining measures Commencing/continuing artificial

nutrition/hydration is inconsistent with good medical practice

No reasonable prospect of regaining capacity

Match the clinical manifestation and symptoms/signs

1. Nephritic syndrome

2. Rapidly progressive glomerulonephritis

3. Nephrotic syndrome

4. Chronic renal failure

5. Isolated urinary abnormalities

a) Acute nephritis, proteinuria, ARF

b) Azotaemia progressing over months/years

c) Haematuria, azotemia, proteinuria, oliguria, oedema, hypertension

d) Glomerular haematuria or subnephrotic proteinuria

e) >3.5g/day proteinuria, haematuria, hypoalbuminaemia, hyperlipidaemia, lipiduria

Match the disease and pathogenesis

1. Postinfectious glomerulonephritis

2. Crescenteric glomerulonephritis type I

3. Crescenteric glomerulonephritis type II

4. Crescenteric glomerulonephritis type III

a) Anti-GBM antibodiesb) Antineutrophil

cytoplasmic antibodies

c) Immune complexes and circulating/planted antigen from bacterial infection

d) Immune complexes as a complication of other nephropathies

Match the nephrotic syndrome and morphology

1. Membranous nephropathy

2. Minimal-change disease

3. Focal segmental glomerulosclerosis

4. Membranoproliferative glomerulonephritis

a) Effacement of podocyte foot processes

b) Thickened GBM + hypercellularity + leukocyte infilitration

c) Focal and segmental sclerosis and hyalinosos

d) Thickened glomerular capillary wall

The following renal biopsy specimen is most likely from a patient with which disease?

a) Focal segmental glomerulosclerosisb) Minimal change nephropathyc) Acute post-infectious glomerulonephritisd) Crescenteric glomerulonephritis

Which is not a treatment you would use for Goodpasture syndrome?

1. Plasmaphoresis2. Corticosteroids3. Cyclophosphamide4. Erythromycin

How do you differentiate glomerular from non-glomerular

haematuria? Glomerular haematuria: contains

bizarrely-shaped cells (each cell is different)

Non-glomerular haematuria: rbcs are smooth disks (all the same)

What is the most common cause of acute renal failure?

Acute tubular necrosis

What are the three phases of ATN?

1. Oliguric phase (tubular obstruction)2. Diuretic phase (tubules not functioning

properly)3. Improving function

Compare the morphological appearances of ischaemic and toxic ATN

Ischaemic: Focal tubular epithelial necrosis Multiple spots along the nephron

Toxic: Acute necrosis Mostly in the PCT

Both: Occlusion of lumen (eosinophilic hyaline casts) Detachment from BM

What are some complications of acute pyelonephritis?

Papillary necrosis Pyonephrosis Perinephric abscess

What are the major risk factors for pyelonephritis?

Being female (more likely to get UTI ) or elderly males (BPH)

Vesicoureteral reflux Intrarenal reflux Catheters Urinary tract obstruction Pregnancy DM Pre-existing renal lesions (scarring, obstruction) Immunosuppression/immunodeficiency

What are the two forms of chronic pyelonephritis

Reflux nephropathy: Due to superimposition of urinary

infection (childhood) on congenital vesicoureteral reflux and intrarenal reflux

Chronic obstructive pyelonephritis: Recurrent infections superimposed on

diffuse/localised obstructive lesions recurrent renal inflamamtion/scarring chronic pyelonephritis parenchymal atrophy

Match the congential anomaly and description

1. Agenesis of the kidneys

2. Dual induction3. Hypoplasia4. Horseshoe kidney5. Congenital

hydronephrosis

a) Distension and dilation of pelvis/calyces usually due to outflow obstruction

b) Either two ureteric buds or the division of a single ureteric bud

c) Failure of one/both kidneys to develop

d) Reduced number of nephrons

e) Fusion of kidneys during ascent

Match the cystic disease and pathological features

1. Adult polycystic kidney disease

2. Childhood polycystic kidney disease

3. Medullary sponge kidney

4. Familial juvenile nephronophthisis

5. Adult-onset medullary cystic disease

6. Simple cysts7. Acquired renal cystic

disease

a) Medullary cysts on excretory radiography

b) Enlarged, cystic kidneys at birth

c) Corticomedullary cysts, shrunken kidneys

d) Large multicystic kidneys, liver cysts, berry aneurysms

e) Cystic degeneration in ESKDf) Single/multiple cysts in

normal-sized kidneysg) Corticomedullary cysts,

shrunken kidneys

What factors may be involved in the higher prevalence and earlier age-of-onset of kidney disease in

indigenous populations? Dec nephron number at birth (? Low birth

weight) Subsequent insults: nephritis, obesity,

early onset DMII Socioeconomic and environmental

determinants

What are the WHO criteria for screening tests?

Important health problem for individual/ community

Accepted treatment/intervention Natural history of the disease should be

understood Latent or early symptomatic stage Screening test or examination Facilities for diagnosis and treatment Policy on whom to treat as patients Early tx should be more beneficial than late tx Economically balanced cost Continued case finding