Renal Medicine

Question 1

What features describe Stage 1 CKD?

Answer 1

eGFR > 90mL/min with evidence of renal damage e.g. proteinuria, haematuria

Question 2

What features describe Stage 2 CKD?

Answer 2

eGFR = 60-89mL/min with evidence of renal damage e.g. proteinuria, haematuria

Question 3

What features describe Stage 3A CKD?

Answer 3

eGFR = 45-59mL/min

Question 4

What features describe Stage 3B CKD?

Answer 4

eGFR = 30-44mL/min

Question 5

What features describe Stage 4 CKD?

Answer 5

eGFR = 15-29mL/min

Question 6

What features describe Stage 5 CKD?

Answer 6

eGFR less than 15mL/min

Question 7

What features describe Stage 1 AKI?

Answer 7

• Serum Creatinine increase >26umol/L in 48h
• OR increase creatinine 1.5 x baseline
• OR urine output less than 0.5mL/kg/hr for at least 6 consecutive hours

Question 8

What features describe Stage 2 AKI?

Answer 8

• Serum Creatinine increase 2-2.9 x baseline

- urine output less than 0.5mL/kg/hr for at least 12hr

Question 9

What features describe Stage 3 AKI?

Answer 9

• Serum Creatinine increase >3 x baseline
• OR creatinine over 354umol/L
• OR urine output less than 0.3mL/Kg/Hr for at least 24hr
• OR anuria for 12h

Question 10

What are some risk factors for developing AKI?

Answer 10

Age >75, CKD, Cardiac Failure, peripheral vascular disease, chronic liver failure, diabetes, drugs, sepsis, poor fluid intake/increased losses, history of urinary symptoms

Question 11

Describe IgA Nephropathy and treatment

Answer 11

a.k.a. Berger’s disease most common cause of glomerulonephritis worldwide due to IgA complex depositon.

Presentation: young male, recurrent episodes of macroscopic haematuria, few days after URTI

Rx: Steroids + cyclophosphamide

Question 12

Describe Post-streptococcal glomerulonephritis, it’s symptoms, treatment

Answer 12

a.k. proliferative GN
Immune complex deposition that occurs 7-14days post strep infection most commonly in children.
Strep antigens deposited on glomerulus –>host response and immune complex formation

Features: Headache, malaise, haematuria, nephritic syndrome, hypertension, low C3, raised ASO (AntiStreptolysin O) titre

Supportive

Question 13

Describe Alport’s syndrome

Answer 13

Alport’s syndrome is an inherited disorder of type IV collagen resulting in abnormal glomerular basement membrane.

Features:
microscopic haematuria
progressive renal failure
bilateral sensorineural deafness
lenticonus: protrusion of the lens surface into the anterior chamber
retinitis pigmentosa
renal biopsy: splitting of lamina densa seen on electron microscopy

Question 14

Define Nephrotic Syndrome, its causes, complications and management

Answer 14

Triad of Proteinuria >3.5g/24h (ACR >250mg/mmol), hypoalbuminaemia and oedema

Primary causes: Minimal change disease, membranous nephropathy, focal segmental glomerulosclerosis, mesangiocapillary glomerulonephritis
Secondary causes: Hepatitis B/C, SLE, diabetic nephropathy, amyloidosis, paraneoplastic, drugs (NSAIDs, penicillamine, anti-TNF, gold)

Complications: susceptibility to infection, thromboembolism, hyperlipidaemia

Management:

• Reduce oedema (Loop diuretic),
• Reduce proteinuria (ACE-inhibitor, Angiotensin-Receptor Blocker)
• Reduce risk of complications (anticoagulate, statin), and Treat underlying cause.

Question 15

Describe Minimal Change Disease and its treatment.

Answer 15

Commonest cause of nephrotic syndrome in children

Biopsy normal under light microscopy.

T-cell and cytokine mediated damaged to GBM leads to polyanion loss and the resultant reduction of electrostatic charge increased glomerular permeability to serum albumin.

Treatment:

• Spontaneous remission is possible, and remission can be induced with steroid therapy but may relapse (steroid-dependent) or be resistant (Steroid Resistant).
• Steroid-resistant disease or steroid-dependent disease can be treated with cyclophosphamide or tacrolimus. 1% progress to ESRF

Question 16

Describe membranous nephropathy

Answer 16

Second most common cause of nephrotic syndrome in adults accounting for 20-30%.

primary or secondary due to malignancy, hepatitis B, drugs (NSAIDs, Gold, Penicillamine) Autoimmune (SLE, Thyroid).

Biopsy shows diffusely thickened GBM with subepithelial deposits of IgG and C3 on immunofluorence. Treatment involves managing nephrotic syndrome.

Question 17

Describe mesangiocapillary glomerulonephritis

Answer 17

May be immune complex mediated or complement mediated and may be due to underlying cause such as Hepatitis C, SLE, monoclonal gammaglobulinopathies.

Biopsy shows mesangial and endocapillary proliferation, thickened GBM and double contouring (tramline) of the capillary walls.

Treat underlying cause and nephortic syndrome. prognosis poor when no underlying cause is found and in patients with ESRF if can reoccur in transplants.

Question 18

Describe focal segmental glomerulosclerosis (FSGS)

Answer 18

Most common cause of nephrotic syndrome in adults.

May be primary (idiopathic) or secondary (Vesicoureteric reflux, IgA nephropathy, vasculitis, Alport’s syndrome, sickle-cell disease, heroin use).

Biopsy shows segmental glomerular scarring and IgM and C3 deposits on immunofluorence.

10% remit spontaneously, may respond to corticosteroids or cyclophosphamide if resistant. Can progress to ESRF and reoccur ~20% of transplants.

Question 19

Describe Rhabdomyolysis, its causes and clinical features.

Answer 19

Rapid muscle breakdown with release of K+, Phosphate, myoglobin, urate, and creatine kinase. This leads to hyperkalaemia and AKI due to renal tubule obstruction by myoglobin.

Causes include trauma (burns, crush injury, uncontrolled seizures), Drugs and toxins (statins, alcohol, ectasy, heroin, neuroleptic malingant syndrome), metabolic (hypokalaemia, myositis) and inheritied muscle disorders (duschenne’s muscular dystrophy, McArdle’s disease)

Clinical features: red-brown urine (visible myoglobinuria), muscle pain, hyperkalaemia, Increased phosphate, plasma CK >1000iU/L, hypocalcaemia, hyperuricaemia.

Question 20

Name some nephrotoxic drugs

Answer 20

NSAIDs, antimicrobials (genatmicin, sulfonamides, penicillins, rifampicin, amphotericin, aciclovir), anticonvulsants (lamotrigine, valproate, phenytoin), omperazole, furosemide, thiazides, ace-inhibitors, ARBs, cimetidine, lithium, iron, cisplatin, radiocontrast.

Question 21

What are some causes of AKI?

Answer 21

Pre-renal: (40-70%) due to renal hypoperfusion e.g. hypotension, renal artery stenosis

Intrinsic renal: (10-50%) tubular (acute tubular necrosis is the commonest, also myeloma, ethylene glycol poisoning, hyperuricaemia, hypercalceamia) glomerular (autoimmune e,g, SLE, Henoch-scholein purpura) Interstitial (infilitration from infection, tumour lysis syndrome) Vascular (vasculitis, HUS/ TTP)

Post-renal: (10-25%) caused by urinary tract obstruction e.g. stones, malignancy (compression

Question 22

What are the complications of AKI?

Answer 22

Hyperkalaemia, pulmonary oedema, uraemia, acidaemia,

Question 23

Describe Haemolytic Uraemic Syndrome (HUS)

Answer 23

Endothelial damage commonly (90%) from E.coli strain O157 leads to thrombosis, platelet consumption and fibrin strand deposition mainly in renal microvasculature. Strands cause mechanical destruction of RBC’s giving triad of haemolysis, thrombocytopenia and AKI. It is most common cause of AKI in children. Clinical features include abdominal pain, bloody diarrhoea and AKI.

Question 24

What are the causes of CKD?

Answer 24

Diabetes (20%), hypertension, glomerulonephritis (commonly IgA nephropathy also SLE, Vasculitis), Unknown

Question 25

Describe Acute Tubular Necrosis (ATN)

Answer 25

Most common cause of AKI, characterised by death of tbular epithelial cells due to ischaemia most commonly caused by hypotension or nephrotoxic drugs. The presence of "muddy brown casts" of epithelial cells found in the urine during urinalysis is pathognomonic for ATN

Question 26

Describe Thrombotic Thrombocytopenic Purpura (TTP)

Answer 26

Overlap with HUS, patients are Thrombocytopenic and have microangiopathic haemolytic anaemia. Other features include AKI, CNS involvement, fever. Due to an genetic or acquired deficiency of protease ADAMTS13 which normally cleaves VonWillebrand multimers Do not infuse platelets

Question 27

Describe transplant rejection

Answer 27

Acute (<6 months): increase serum creatinine, fever, graft pain. Immune cell infiltrate and tubular damage. Rx - high dose IV methylprednisolone. if resistant - anti-thymocyte globulin, OKT3 Chronic (>6 months): interstitial fibrosis and tubular atrophy. Gradual increase in creatinine and proteinuria. Rx - general management of chronic renal failure (not responsive to immunosuppression)

Question 28

Describe renal biopsy, its indication, pre procedure checks, contraindications and complications

Answer 28

Patients lay on their front, local anaethetic used and core biopsy taken. Bed rest on back for minimum of 6h Indications: - unexplained AKI or CKD - acute nephritic syndrome - unexplained proteinuria or haematuria - suspected transplant rejection - systemic disease associated with kidney dysfunction Pre procedure check: FBC, clotting, group and save. obtain written consent. Ultrasound to delineate anatomy (Horseshoe kidney?, two kidney? Size?). Stop anticoagulants (asprin 1 wk, wafarin 3 days, LMWH 1 day) Contraindications: - abnormal clotting - hypertension greater than 160/90mmHg - single kidney - CKD with small kidneys (less than 9cm) - uncooperative patient - horseshoe kidney - renal neoplasms. Complications: - Bleeding, macroscopic haematuria occurs in 1/10 - Bleeding requiring transfusion in 1/100 - nephrectomy rare

Question 29

What are the indications of dialysis?

Answer 29

- hyperkalaemia unresponsive to medical treatment or in an oliguric patient - Pulmonary oedema unresponsive to medical treatment - uraemic complications such as pericarditis or encephalopathy - severe metabolic acidosis unresponsive to treatment (pH

Question 30

Describe Renal tubular acidosis, its types, and treatment.

Answer 30

Is a metabolic acidosis due to impaired acid secretion by the kidney. There is a hyperchloraemic metabolic acidosis with normal anion gap. Types: There are 4 types and type 3 is a combination of type 1 and 2. - Type 1 (distal) RTA is due to an inability to excrete H+ and generate acidic urine in the distal tubule. - Type 2 (proximal) is due to a 'bicarbonate leak' a defect in HCO3 reabsorption in the proximal tubule resulting in excess HCO3 in the urine. - Type 4 (hyperkalaemic) is due to hyporeninaemic hypoaldosteronism. hypoaldosteronism causes hyperkalaemia and acidosis. Treatment: is with bicarbonate.

Question 31

Describe nephritic syndrome and its causes.

Answer 31

Nephritic syndrome includes haematuria, proteinuria, hypertension and ureamia. Primary causes include IgA nephropathy and mesangiocapillary glomerulonephritis. Secondary causes include post-streptococcal, vasculitis, SLE, Goodpastures, cryoglobulinaemia.

Question 32

Describe Hyperkalaemia, its signs, symptoms, causes and treatment

Answer 32

Plasma potassium >5.5mmol/L, increased potassium leads to myocardial hyperexcitability leading to ventricular fibrillation and cardiac arrest. Signs + symptoms: Fast irregular pulse, chest pain, weakness, palpitations, light-headedness. ECG: tall tented T waves, small p waves, wide QRS, VF. Causes: Artefact - haemolysis, contamination, thrombocythaemia, delayed analysis Excessive intake - oral,/parenteral, massive transfusion Transcellular movement (ICF -> ECF) - metabolic acidosis (DM), insulin storage, rhabdomyolysis, burns Decreased excretion: oliguric renal failure, K+ sparing diuretics, addison's disease, drugs (e.g. ACEi, NSAIDs, ARB, Suxamethonium) Treatment: Monitor ECG If K+ > 6.5 mmol/l or if there are ECG changes: - 10ml 10% calcium gluconate IV over 2 mins - 50ml 50% glucose + 10U insulin (actrapid) - salbutamol 5mg nebs - Calcium resonium 15g PO or 30g PR - Haemofiltration If non-urgent - treat underlying cause, review medications; give calcium resonium 15g/8hr PO

Question 33

Describe Syndrome of Inappropriate ADH secretion (SIADH), it's causes, and management.

Answer 33

A cause of hyponatraemia and decreased Urine output, SIADH consists of: -concentrated urine (Na+ > 20mmol/L, osmalility >100mosmol/kg) -hyponatraemia (plasma Na less than 125mmol/mL) -low plasma osmolality (less than 260mosmol/kg) in the absence of hypovolaemia, oedema or diuretics Causes: - malignancy: Lung small cell, pancreas, prostate, thymus, lymphoma - CNS disorders: Menigoencephalitis, abscess, stroke, subarachnoid or subdural haemorrhage, head injury, neurosurgery, guillain-barre, SLE, Vasculitis - Chest disease: TB, pneumonia, abscess, aspergillosis, small cell lung cancer - Endocrine: Hypothyroidism - Drugs: Sulfonylureas, SSRIs, tricyclics, carbamazepine, vincristine, cyclophosphamide. - Other: Acute intermittent porphyria, trauma, abdominal or thoracic surgery, symptomatic HIV. Management: -identify and treat the cause - fluid restrict Consider salt +/- loop diuretics

Question 34

What are the causes of Hyperuricaemia?

Answer 34

Drugs: Cytotoxics, Thiazides, Loop Diurectics, pyrazinamide Increased Cell Turnover : lymphoma, leukaemia, psoriasis, haemolysis, rhabdomyolysis, tumour lysis syndrome Reduced Excretion: primary gout, chronic kidney disease, lead nephropathy, hyperparathyroidism, pre-eclampsia

Question 35

Describe Acute Urinary Retention, its causes, symptoms, and management

Answer 35

Causes: prostatic obstruction (usual cause in males), urethral strictures, anticholinergics, alcohol, constipation, post-op, infection, neurological (cauda equina syndrome), carcinoma. Symptoms: Tender bladder, anuria, dull percussion of bladder. Management: - MSU, U+E, FBC, and PSA to help identify cause. - Conservative management: tricks to aid voiding such as analgesia, privacy on hospital wards, ambulation, standing to void, voiding to sound of running taps or in a hot bath. - Other wise Catheterise and start an alpha-blocker e.g. Tamulosin. - Monitor for post-obstructive diuresis, in acute phase after relief of the obstruction, the kidneys produce a lot of urine, match input to output. - TWOC

Question 36

Describe Hypokalaemia, it's signs and symptoms, causes, and management

Answer 36

If K+ less than 3.5mmol/L Signs and Symptoms: Muscle weakness, hypotonia, hyporeflexia, cramps, tetany, palpitations, light-headedness (arrhytmias), constipation ECG - small/inverted T waves, prominent U waves, long PR interval, depressed ST segments Causes: - GI losses: diarrhoea, vomiting, purgative and liquorice abuse, pyloric stenosis, rectal villous adenoma, intestinal fistula - Renal losses: Conn's syndrome, diuretics - Redistribution: Cushing's/steroids/ACTH, B-agonist, alkalosis Othrs: Renal tubular acidosis 1 +2, hypomagnesaemia Management: - mild (>2.5, asymptomatic): oral K+ supplements (Sando K 2 tabs/8hr). Review after 3 days - Severe (<2.5, symptomatic): IV potassium (max 10mmol/hr)

Question 37

Describe Urinary Tract Calculi (aka kidney stones, nephrolithiasis), it's presentation, investigations and management.

Answer 37

Stones form in collecting ducts and may be deposited anywhere from the renal pelvis to the urethra. Signs and symptoms: Asymptomatic Renal colic (severe waxing and waning loin pain radiating to the groin or thigh, with fever or vomiting), Renal obstruction (loin pain), UTI can co-exist (burning sensation, increased urinary frequency), and pyelonephritis (fevers, rigours, loin pain, nausea and vomiting). Investigations: - Bloods: FBC, U+E, Ca2+, PO43-, glucose, bicarbonate, urate. - Urinalysis - MSU: MC+S - Imaging: USS, Non-contrast CT (IVU, KUB Xray) Management: -Analgesia e.g. Diclofenac 75mg IV/IM or 100mg PR -Antibiotics e,g, Cefuroxime 1.5mg/8h IV or gentamicin if infection -Stones <5mm pass spontaneously, increase fluid intake -Stones >5mm or pain not resolving require medical expulsion therapy with nifedipine 10mg/8h or tamsulosin 0.4mg/d extracorporeal shockwave lithotripsy (SEs renal injury, may also cause hypertension and DM. Percutaneous nephrolithotomy

Question 38

Describe Polycystic Kidney disease, symptoms, and management.

Answer 38

Autosomal dominant, 85% have a mutation in PKD1 on chromosome 16 and 15% in PKD2 in chromosome 4. The first type present with renal failure earlier. Symptoms: Renal enlargement with cysts causing abdominal pain +/- haematuria, and hypertension. Extrarenal symptoms: liver cysts, SAH (berry aneurysms), mitral valve prolapse, ovarian cysts, diverticular disease. Management: - General: Increase water intake, decrease Na+, decrease caffeine. Monitor U+E and BP (aim <130/80) Genetic counselling. MRA screening - Medical: Rx hypertension agreesively. Rx infection. - Surgical: if pain, recurrent bleeds or infection - laparoscopic cyst removal or nephrectomy For ESRF - Dialysis/ transplantation

Question 39

Describe Bartter's syndrome and its symptoms.

Answer 39

An autosomal recessive cause of severe Hypokalaemia due to defective chloride absorption at the NKCC2 in the ascending loop of Henle. It is Socrates with normotension unlike other causes of Hypokalaemia such as Conn's, Cushings and Liddles. Symptoms: Polyhydraminos in utero, Failure to thrive, Polyuria, polydipsia, Hypokalaemia, normotension, weakness.

Question 40

Types of Stones from urinary tract calculi

Answer 40

Calcium oxalate (75%) - radio-opaque Magnesium ammonium phosphate (Triple phosphate/struvite) (15) - UTI - proteus, staghorn calculi, radio-opaque Urate - hyperuricaemia, smooth,brown, radiolUcent Brushite Cysteine - Renal tubular defects, yellow, crystalline, semi-opaque Hydroxyapatite Calcium phosphate Mixed