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  1. What investigations would you do to assess whether AKI was due to pre-renal or ATN?
    • urinary sodium. in pre-renal failure kidneys attempt to preserve sodium to preserve volume.
    • pre-renal would respond to a fluid challenge, ATN wouldnt.
    • pre-renal would have a disproportionate rise in urea:creatine ratio (due to hypovolaemia and dehydration causing high urea).
    • blood or protein in urine suggests an inflammatory process within the kidneys. (tubular casts = ATN, red cells casts = GN, eosinophils = AIN).
    • urine osmolality is high >500 in pre-renal. in ATN there is loss of ability to concentrate the urine with a lower <300 urine osmolality.
  2. Why is serum creatinine limited for use in assessing AKI?
    the level can remain in the normal range despite a drop of 50% in renal function
  3. In AKI what is suggested by markedly raised myoglobin and CK?
  4. What could be the mechanism of breathlessness in renal disease?
    • acidosis
    • anaemia
    • fluid retention (pulmonary oedema, pleural effusion)
  5. Causes of red/brown urine?
    • blood
    • porphyria
    • rhabdomyolysis
    • rifampicin
    • phenytoin
    • beetroot
    • maple syrup urine disease.
    • dark urine - obstructive jaundice
  6. Renal causes of haematuria?
    • haemophilia
    • sickle cell
    • iga nephropathy
    • alports
    • SLE
    • GN (rapidly progressive)
    • renal cell ca
    • transitional cell ca
    • stones
    • tb
    • papillary necrosis
    • hereditary haemorrhagic telangiectasia
    • AV malformations
    • PCKD.
  7. What is Fabry's disease?
    • x linked recessive inborn error of metabolism. Along with Gaucher's it is one of the most prevelent inborn errors of metabolism.
    • female carriers exist and can exhibit mild symptoms
    • classical manifestation: males are slight with delayed puberty. early burning and paraesthesia in extremities.
    • small punctate red-black telangiectasias (angiokeratomas) occur on skin in bathing suit distribution.
    • eye involvement
    • heart - MI, arrhythmias in 30s.
    • GI - nausea, diarrhoea, weight loss
    • eventually require dialysis and renal transplant.
  8. Define nephrotic syndrome
    • oedema
    • plasma albumin <30g/l or 3g/dl
    • >3g urinary protein loss/24h
  9. first line investigation in Nephrotic syndrome?
    renal biopsy
  10. Complications of nephrotic syndrome?
    • thrombosis due to increased vwbf, fV, protein C. platelets become hypercoagulable.
    • increased hypercholesterolaemia can rarely cause eruptive xanthomata.
    • bacterial infections more common due to reduced igG production.
  11. Causes of nephrotic syndrome?
    • minimal change
    • iga
    • membranoproligerative GN
    • Membranous GN
    • Focal and segmental GS.
    • Gold penicillamine, NSAIDS.
    • DM
    • Amyloidosis
    • SLE
    • HIV and HCV associated nephropathy
  12. Management of FSGS?
    • This often presents as nephrotic syndrome, and has a variety of causes.
    • primary - steroids
    • secondary (e.g. HIV, Heroin use, sickle cell, obesity, reflux) are due to hyperfiltration injury and require ACEi or A2RB.
  13. How does the pathophysiology of thin basement membrane disease differ from Alport's syndrome?
    • Both effect the GBM however Alports is X-linked dominant and has an abnormality of type IV collagen.
    • thin basement membrane disease has no abnormality but the membrane is thin and leads to isolated haematuria commonly. If this occurs in families it is called benign familial haematuria (AD).
  14. primary cause of nephrotic syndrome in adults? What causes it and what is seen on biopsy?
    • membranous nephropathy.
    • immune-mediated (idiopathic or secondary e.g. autoimmune disease - SLE, Hashimotos, infection, penicillamine, gold, NSAIDS, malignancy)
    • characterised by immune complex localisation in subepithelial zone of glomerular capillaries.
  15. A patient presents with recurrent renal calculi, and episodes of haematuria. you notice they have a left upper limb more than 10% larger than the right.
    What is the most likely renal cause of the recurrent calculi?
    • medullary sponge kidney
    • Medullary sponge kidney (MSK) is a congenital disorder that can affect one or both kidneys, or only part of one kidney. There are ectatic and cystic changes of the medullary and papillary collecting ducts.1 The names tubular ectasia and cystic dilatation of the collecting ducts have been suggested as alternatives for this condition because the medulla does not actually appear like a sponge. It is bilateral in 70% of cases.2 Cysts can be 1-7 mm in diameter. Cyst formation is commonly associated with the development of small calculi within the cyst. The rest of the kidney is usually normal unless affected by complications such aspyelonephritis or obstruction secondary to renal calculi.
    • Congenital hemihypertrophy: this is the most frequent association. There is enlargement of a limb or one side of the body compared with the contralateral side beyond the limits of normal variation. 10% of people with congenital hemihypertrophy have MSK.2
  16. Top 5 causes (in order) or chronic renal disease leading to ESRF?
    • 1. Diabetic nephropathy (37%)
    • 2. hypertension (25%)
    • 3. GN and other glomerular disease e.g. vasculitis such as SLE.
    • 4. PCKD
    • 5. Tubulointestitial disease e.g. pyelonephritis, medication induced nephrotoxicity.
  17. A patient presents with arthralgia, mouth ulcers and alopecia. o/e there is a discoid rash on the head and neck. bloods reveal a raised ANA, and low C3, C4. Hypertension prompts further bloods and urinalysis revealing proteinuria and a GFR of 58.
    What is likely to be seen on biopsy of the kidney?
    lupus nephritis

    • - initially mesangial deposits (class II)
    • - mesangial hypercellularity (IIb)
    • - focal segmental proliferative GN (III)
    • - diffuse proliferative GN (IV)
    • - membranous GN (v)

    crescents usually seen in types III and IV.
  18. How does membranous GN present and how is it investigated?
    • membranous GN is a common immune-mediated GN and one of the leading causes of nephrotic syndrome in adults.
    • presents with proteinuria and occasionallly hypertension.
    • ix with biopsy.
  19. Describei the categories used for chronic kidney disease.
    • Stage 1: GFR >90 ml/min despite Kidney damageMicroalbuminuria present
    • Stage 2: Mild reduction (GFR 60-89 min/min)GFR of 60 may represent 50% loss in functionParathyroid Hormone starts to increase
    • Stage 3: Moderate reduction (GFR 30-59 ml/min)Calcium absorption decreasesMalnutrition onsetAnemia secondary to Erythropoietin deficiencyLeft Ventricular Hypertrophy
    • Stage 4: Severe reduction (GFR 15-29 ml/min)Serum Triglycerides increaseHyperphosphatemiaMetabolic AcidosisHyperkalemia
    • Stage 5: Kidney Failure (GFR <15 ml/min)Azotemia
  20. 2 Formula for eGFR?
    • Cockcroft-Gault
    • MDRD (modification of diet in renal disease score)
  21. 6 things you are looking for in kidney USS to support a CKD diagnosis?
    • 1. veins and arteries for thrombosis or RAS
    • 2. nephrocalcinosis
    • 3. hydronephrosis
    • 4. renal mass or complex cysts (suggests malignancy)
    • 5. enlarged kidneys e.g. renal tumours invasive disease, nephrotic syndrome related disease.
    • 6. asymmetric kidney size or scarring - vascular disease (chronic RAS), urological disease, tubulointerstital disease, scarring - previous UTI or infection in females.
    • 7. small hyperechoic kidneys = chronic kidney disease.
  22. Typical UAE findings in stage IV chronic kidney disease?
    • hyperkalaemia (or hypo possible)
    • acidosis
    • hypocalcaemia
    • hyperphosphataemia
    • decreased serum protein
    • anaemia
    • uraemia
  23. MEN I?
    • primary hyperparathyroidism
    • pituitary adenoma e.g. prolactin, GH, ACTH (cushings)
    • pancreatic islet tumours e.g. insulinoma and hypoglycaemia, gastrinoma and peptic ulcers.
    • zollinger-ellison syndrome
  24. MEN II?
    • primary hyperparathyroidism
    • phaeochromocytoma
    • medullary thyroid carcinoma
  25. A patient presents with sudden onset headache, diplopia and worsening tunnel vision. He has a past medical history of hyperparathyroidism, recurrent hypoglycaemia currently under investigation and peptic ulcers. What diagnosis may he have, and what complication has he just suffered?
    hyperPTH, pancreatic islet tumour (insulinoma) and gastrinoma suggest MEN I syndrome. Another association with this is pituitary adenoma which can remain asymptomatic in a large proportion. A complication is pituitary apoplexy where there is haemorrhage into an existing tumour (80% are asymtpomatic until this point). management is immeadiate replacement of pituitary factors e.g. steroids and surigcal decompression may be necessary.
  26. moa of hyperacute renal graft rejection?
    • circulating antibodies in recipient (due to previous sensitization) attack antigens present in donor kidney.
    • How does this occur? normally ABO or HLA antibodies. error in cross match e.g. patient is cross matched before being given a transfusion which then causing sensitization to a blood antigen.
  27. What is the most common cause of acute rejection episodes post renal transplant?
    • cellular rejection. (occurs around a week after transplant which was previously functioning).
    • There is a diffuse infiltrate of T cells, macrophages causing destruction of tubular cells and basement membrane (appears like AIN from drugs). COMMONLY DUE TO MEDICATION NON COMPLIENCE.
  28. What causes late graft dysfunction?
    • chronic rejection (ie. evidence of chronic glomerular, intestitial and vascular damage months to years down the line).
    • chronic calcineurin inhibitor toxicity (cyclosporin toxicity causing tubular damage and interstitial fibrosis. can also occur acutely)
    • recurrent glomerular disease (familial HUS, IGA, focal segmental glomerulosclerosis).
    • post transplant lymphoproliferative disorder (b cell clonal expansion most commonly associated with EBV and causing an infectious mono type picture).
  29. Which pathogen is most concerning following renal transplant?
    • CMV.
    • ciclosporin inhibits T cell formation and therefore infection post transplant is with those seen in HIV - CMV, Herpes simplex and zoster, EBV, HHV8, Hep B/C, JC virus (progressive multifocal leucoencephalopathy).
    • cmv infection can occur 4-8 weeks post op without anti-viral prophylaxis (which is given in high risk patients) and causes fever, leucopenia and thrombocytopenia.
  30. Why do you get a metabolic alkalosis in hypokalaemia?
    because Hydrogen ions shift from the extracellular to intracellular space to maintain the membrane potential in the abcence of potassium.
  31. a 10 year old presents with thirst and bed wetting. Investigations revealed low potassium, sodium and an alkalosis. Blood pressure is normal. What is the diagnosis?
    • Bartter syndrome
    • There are five gene defects known to be associated with Bartter syndrome. The condition is present from before birth (congenital).The condition is thought to be caused by a defect in the kidney's ability to reabsorb sodium. Persons with Bartter syndrome lose too much sodium through the urine. This causes a rise in the level of the hormone aldosterone and makes the kidneys remove too much potassium from the body. This is known as potassium wasting. The condition also results in an abnormal acid balance in the blood called hypokalemic alkalosis.

    This disease usually occurs in childhood. Symptoms include: ConstipationGrowth failureIncreased frequency of urinationLow blood pressureKidney stoneMuscle cramping and weakness

    The diagnosis of Bartter syndrome is usually suspected by finding low levels of potassium in the blood. The potassium level is usually less than 2.5 mEq/L. Unlike other forms of kidney disease, this condition does not cause high blood pressure and there is a tendency toward low blood pressure. Other signs of this syndrome include:High levels of potassium, calcium, and chloride in the urineHigh levels of the hormones renin and aldosterone in the bloodLow blood chlorideMetabolic alkalosisThese same signs and symptoms can also occur in people who have taken too many diuretics or laxatives. Urine tests can be done to rule out these causes.In Bartter syndrome, a biopsy of the kidney typically shows too much growth of kidney cells called the juxtaglomerular apparatus. However, this is not found in all patients, especially in young children.
  32. What is the mechanism of renal osteodystrophy in chronic renal failure?
    • reduced vitamin D activity leads to decreased calcium absorption and hypocalcaemia. phosphate retention occurs causing hyperphosphataemia.
    • Secondary hyperparathroidism occurs.
    • causes osteoclastic breakdown of bone
    • this causes osteomalacia and osteitis fibrosa cystica.
  33. Summarise bloods in each of the following:
    Addisons disease
    Bartters syndrome
    Liddles syndrome
    Fanconi syndrome
    • Addisons: low sodium, raised potassium, hypotension, acidosis
    • Bartters: low sodium, low potassium, normotension, alkalosis
    • Liddles (pseudoaldosteronism): high sodium, low potassium, low renin/aldosterone, hypertension. (ie. same profile as Cushings, but aldosterone is low - caused by a sodium channel mutation)
    • Fanconi: Defect in proximal tubule function that can be inherited or acquired. glucose, amino acids, uric acid, phosphate and bicarb are excreted into urine. principally causes osteomalacia or rickets due to phosphate wasting.
  34. What is the difference between type 1 and type 2 RTA?
    • Both are a metabolic acidosis due to failure to acidify urine. Type 1 occurs at the distal tubule (fails to excrete ammonium)
    • type 2 occurs at the proximal tubule where bicarbonate wasting occurs.

    both give an elevated chloride, a low bicarb (as its either wasted by kidney or buffering acidosis), normal anion gap acidosis.
  35. 4 major symptoms of HSP?
    • Purpura
    • abdo pain
    • arthritis
    • haematuria
  36. Why are HSP and IgA nephropathy similar?
    both have raised serum IgA, and identicle findings on renal biopsy. iga affects predominantely young adults (and only the kidneys) whereas HSP affects young children (and skin, GI tract, scrotum, joints)
  37. How do platelet and coagulation studies differ in HSP, ITP and TTP?
    • HSP - normal platelets and clotting (as small vessel vasculitis)
    • ITP - low platelets normal clotting
    • TTP - low platelets, deranged clotting, anaemia and schistosytes due to haemolytic anaemia.
  38. How might TTP present?
    • thrombocytopenic purpura
    • fever
    • renal disease
    • haemolytic anaemia
    • leading to neuro signs e.g. seizures, comas, and death (80% mortality in 3 months if untreated).
  39. How is TTP managed?
    • plasmapheresis (FFP exchange)
    • Steroids and aspirin can be given as an adjunct.
    • refactory cases: splenectomy, gammaglobulin, vincristine.
  40. Most common stones to be formed post infection?
    • magnesium ammonium phosphate (struvite)
    • calcium phosphate
    • v. large stones may be formed causing staghorn calculi.
    • more common in people with recurrent infection due to structural abnormality
    • organisms are proteus, e coli, klebsiella
    • urine becomes alkaline due to bacteria spliting urea to ammonia and co2. struvite crystals found on urinalysis.
  41. What auto recessive condition should be considered in a young adult presenting with recurrent renal stones?
    • cystinuria.
    • AR
    • cystine stones formed. may have large stag horn calculi.
    • males effected more severely than females.
    • mx with increased fluid intake and alkalinization of urine. some patients have recurrent infection/stones and develop ESRF.
  42. Complications of haemodialysis?
    • immeadiate anaphylaxis (to membrane)
    • early reaction (30-60mins)
    • dialysis hypotension
    • hypertension
    • arrhythmia and sudden death (80% due to VF, more common in T1DM). made worse by hypokalaemia, hypocalcaemia and hypomagnesaemia seen post dialysis.
    • 25% report cramps towards end due to low calcium and magnesium concentrations.
    • Fistula blockage.
    • long term complications: CAD, ectopic calcification (skin, joints, lungs, myocardium, LVH, amyloidosis (usually starts in hands as carpal tunnel syndrome, shoulders hips and knees can be effected with severe aching), renal bone disease
  43. Complications of peritoneal dialysis?
    • infection
    • catheter migration (due to being enmeshed in omentum). constipation can cause migration (common in PD)
    • peritnoneal leak (e.g. sub cut)
    • hernia
    • long term complications: CAD, ectopic calcification (skin, joints, lungs, myocardium, LVH, amyloidosis (usually starts in hands as carpal tunnel syndrome, shoulders hips and knees can be effected with severe aching), renal bone disease
  44. What part of the body has to be excised in most patients after 10 years of dialysis?
    • parathyroid glands.
    • hyperparathyroidism occurs due to chronically low calcium. this is managed initially with vitamin D analogues, and manipulation of dialysate calcium concentration.
    • when pth glands become too large they act autonomously.
    • ectopic calcification of skin, muscle, joints etc, hypercalcaemia, myopathy, tendon rupture or bone fracture are all indications for surgical parathyroidectomy.
Card Set:
2012-02-23 13:42:51
kidneys nephrology GN

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