Renal Quizz

For a free chocolate, courtesy of Shravya,Can you link this ECG to a renal cause?

Ans at END

Which part of the nephron does this?

• Reabsorption only and 65% of reabsorption occurs here.

• Majority of H and K secretion occurs here.• 2 Sections subject to hormonal control.

In patients with CRF and HT due to bilateral renal artery stenosis, which of the following agens is MOST LIKELY

to reduce GFR?

• A. Beta blockers• B. Ca anatagonists• C. ACE inhibitors• D Nitrates• C corticosteroids

All of the following can result from hypokalaemia except:

A. Cardiac arrhythmiaB. B. Intestinal stasisC. C. Tall peaked T waves in the ECGD. D. Muscular weaknessE. E. Polyuria

Ans• Hypokalaemia would cause flattened T waves and U waves

At what GFR you get ESRF

Major causes of CRF

• What is a major congenital cause?• Major vascular cause?• Name 2 others.

• Congenital = polycyctic kidney disease• HT• Diabetic nephropathy, reflux nephropathy

(chronic pyelonephritis)

Which of these is not a manifestation of CFR

• Inc urea and protein metabolites• Na and water retention• Dec H+ excretion• Dec phosphate excretion• Dec EPO synthesis• Altered sex hormone production/metabolism• Altered lipid metabolism

• Ans: trick question – they all are manifestations. High five!!!

What is the biochem cause?

Does good urine output = good renal function?

ANS

• NO. • Failure of tubular reabsorption may lead to

high urine volume. • Tubular dysfunction to some extent always

accompanies glomerular disease, so urine output is not a useful guide to renal Fx.

Important Cx of CRF

• List a bone manifestation.• List a couple of Cardiac manifestations• A haematological manifestation• List 3 GI manifestations• A Endocrine manifestation• Skin manifestations?• Nervous system?

• Renal bone disease.• Uraemic pericarditis is common. Renal failure

increases incidence of CVD up to 16X• Anaemia. EPO• Reflux oesophagitis, inc risk of peptic ulceration,

inc risk of acute pancreatitis (inc serum level of amylase may be found in CRF due to retention of amylase normally exreted inurine.

• Gout due to urate retention, insulin abnormalities (reduced degradation of insulin), lipid metabolism abn – impaired clearance of TAG and hypercholesterolaemia

• Pruritis and itch due to accumulation of nitrogenous waste.

• Nervous system: uraemia can cause unusual combinations of dec cerebral fx and seisures and coma.

ARF

• Some complications are:– Na and water retention.– Electrolyte disturbances – ie hyperkalaemia– Uraemia

• How would each of these manifest in a pt?

ans

• Pulmonary oedema, HT, LV failure• Arrhythmias• Pruritis, CNS manifestations, pericarditis, etc.

ADPKD

• Austosomal dominant kidney disease is the most common inherited nephropathy.

• Multisystematic and progressive disorder characterised by formation and enlargment of renal cysts in the kidney and other organs (liver, pancreas, spleen).

• What is the most common clinical presentation??

Clinical presentation of ADPKD

• Pain in abdomen, flank or back – almost found universally in all pt with ADPKD.

• Renal – palpable, bilateral mass may be found.• CV – HT one of the most common early

manifestation, often precedes renal dysfunction. Also valvular disease occurs in25% of pt, most commonly mitral valve prolapse and aortic regurg.

• What are pt with ADPKD at risk of?? (classic question)

Cerebral aneurysms

• 4x inc risk of subarachnoid or cerebral haemorrhage from a ruptured intracranial aneurysm, as compared to general population.

• CT

• What would you use to diagnose ADPKD?– Ultrasound

Mx of ADPKD

• Largely supportive• Control BP• Treat infections (the cycts may get infected)• Reduce abdominal pain (the thing they will

likely present with), but avoid NSAID.• Surgical – – drainage of infected cysts– Alcohol sclerosis to reduce size of cyst.

A. Rapidly progressive GN/ Crescenteric GNB. Focal segmental GNC. Diffuse proliverative GN (post strep)D. Membranoproliferative GNE. Membranous GNF. Minimal change GNG. IgA nephropathyH. Focal segmental glomerulosclerosis

Not a ‘true’ GN – there is no inflammatory change within the glomeruliFusion of glomerular epithelial cell foot processesMost common in??? Causes 80-85% of nephrotic syndrome in X.

• Thickening of basement membrane due to immune complex deposition is the main feature. • Causes/ associations: SLE, Hep B, malignancy (GIT and bronchus)• Presents as Nephrotic syndrome

A. Rapidly progressive GN/ Crescenteric GNB. Focal segmental GNC. Diffuse proliverative GN (post strep)D. Membranoproliferative GNE. Membranous GNF. Minimal change GNG. IgA nephropathyH. Focal segmental glomerulosclerosis

• Presents with signs of renal failure• There is a proliferation of epithelial cells and infiltration of macrophages in Bowmans space.• Associated with severe glomerular damage and quick renal failure• Rare, but occurs with Goodpasture’s syndrome, ANCA +ve vasculatitis, SLE, TTP/HUS

A. Rapidly progressive GN/ Crescenteric GNB. Focal segmental GNC. Diffuse proliverative GN (post strep)D. Membranoproliferative GNE. Membranous GNF. Minimal change GNG. IgA nephropathyH. Focal segmental glomerulosclerosis

• An acute inflammation of all glomeruli.• Circulating antigen-antibody complexes deposits in the glomerulus• Presents as nephritic • Commonly presents how many weeks post-strep infection?

A. Rapidly progressive GN/ Crescenteric GNB. Focal segmental GNC. Diffuse proliverative GN (post strep)D. Membranoproliferative GNE. Membranous GNF. Minimal change GNG. IgA nephropathyH. Focal segmental glomerulosclerosis