Renal

Question 1

Renal function tests

Blood

Answer 1

 FBC – Anaemia, infection, allergic reactions,
 Haematinics – Iron/Folate/B12 deficiency
 U&Es – Potassium, Urea, Creatinine, Bicarbonate
 Bone profile – Calcium, Phosphate, PTH, Alkaline Phosphatase
 CRP – Infection/Inflammation
 HbA1c – Diabetic control

Question 2

Renal function tests

Urine

Answer 2

 Urine Dipstick – Infection (leukocytes, nitrites); Glomerular pathology (blood, protein)
 Urine Protein:Creatinine Ratio – Quantifies the amount of all protein in the urine
 Urine Albumin:Creatinine Ratio – Quantifies just albumin (good for diagnosing and monitoring diabetic
nephropathy)
 Urine microscopy, culture and sensitivity

Question 3

Renal function tests

Imaging

Answer 3

US KUB – look for peri-nephric collection, size of kidneys, corticomedullary differentiation, hydronephrosis

Question 4

Metabolic alkalosis causes

Answer 4

 GI losses
o Diarrhoea
o Vomiting

  Anion Gap = 145 – (107+13) = 25   Renal losses
o  Primary hyperaldosteronism
o  Tubular transporter defects
o  Diuretics
  Intracellular shift
o  Hypokalaemia

Question 5

Anion gap

Answer 5

Anion gap = sodium - (chloride + bicarbonate)

Normal = 8-12

Question 6

High anion gap

Acidosis due to increased acid

Answer 6

Lactic acidosis - anaerobic exercise, sepsis, organ ischaemia
Ketoacidosis - diabetic, alcohol abuse, starvation
Toxins - ethylene glycol, methanol, isoniazid, aspirin, salicylate
Renal failure

Question 7

Normal anion gap

Acidosis due to reduced alkali

Answer 7

GI losses of HCO3 - vomiting, diarrhoea
Renal losses of HCO3 - renal tubular acidosis, mineralocorticoid deficiency (Addison’s)
Toxins - ammonium chloride, acetazolamide

Question 8

Hypernatraemia

Answer 8

Usually due to water deficit.
 Causes cellular dehydration (osmotic drag).
 Creates vascular shear stress (bleeding and
thrombosis)

Question 9

Hypernatraemia

Symptoms

Answer 9

thirst, apathy, irritability, weakness,

confusion, reduced consciousness, seizures, hyperreflexia, spasticity & coma.

Question 10

Hypovolaemic High Na

Answer 10

 Renal free water losses (Osmotic diuresis [NG feed etc], loop diuretics, intrinsic renal disease)
 Non-Renal free water losses (Excess sweating, Burns,
Diarrhoea, Fistulas)

Question 11

Euvolaemic high Na

Answer 11

 Renal Losses (Diabetes Insipidus, Hypodipsia)

 Extra-Renal Losses (Insensible, Respiratory losses)

Question 12

Hypervolaemic high Na (sodium gains)

Answer 12

Primary hyperaldosteronism, Cushing’s Syndrome,
Hypertonic dialysis, Hypertonic Sodium Bicarbonate,
Sodium Chloride tablets

Question 13

Hypernatraemia

Diabetes Insipidus

Answer 13

(differential = psychogenic polydipsia)
– dilute urine (Urine osmolality <300)
Polydipsia and polyuria – not always hypernatraemic
Impaired release of ADH (Cranial DI)

Question 14

Hypernatraemia - Diabetes Insipidus

Causes

Answer 14

Causes - Trauma/post-op, tumours, cerebral sarcoid/TB, infection (meningitis/encephalitis), cerebral
vasculitis (SLE/Wegener’s)
Resistance to ADH (nephrogenic DI)
Causes - Congenital, Drugs (lithium,
amphoterecin, demeclocycline), hypokalaemia,
hypercalcaemia, tubulointerstitial disease

Question 15

Hypernatraemia - Diabetes Insipidus

Treatment

Answer 15

Generally - free water

Question 16

Hyponatraemia

Answer 16

Low Na causes decreased perception and gait disturbance, yawning, nausea, reversible ataxia, headache, apathy, confusion, seizures, coma.

Question 17

Hyponatraemia - causes

Answer 17

Pseudohyponatraemia – occurs with high lipids, myeloma, hyperglycaemia, uraemia etc.

Question 18

Hyponatraemia - investigations

Answer 18

plasma osmolality (if normal or raised
then pseudohyponatraemia),
hypokalaemia/hypomagnesaemia potentiates ADH release, Urine sodium (if <20 then non-renal salt losses, if >40 then SIADH) (diuretics may confound), TSH and 9am cortisol, Calcium, albumin, glucose, LFT, CT head or chest if
suspect SIADH.

Question 19

Hypovolaemic hypernatraemia

Answer 19

Renal loss [Urine Na+ >20mmol/L]
 Diuretics (thiazides), Osmotic diuresis (glucose, urea in
recovering ATN), Addison’s disease (mineralocorticoid
deficiency)
Non-renal loss [Urine Na+ <20mmol/L]
 Diarrhoea, Vomiting, Sweating, Third space losses
(burns, bowel obstruction, pancreatitis)
Treatment – give IV fluids (0.9% NaCl at 1-3ml/kg/hour) Give K if necessary

Question 20

Euvolaemic hyponatraemia

Answer 20

Hypothyroidism, Primary polydipsia – (if urine
osmolality <100), Glucocorticoid deficiency – adrenal
insufficiency, SIADH

Question 21

Hyponatraemia - SIADH

Answer 21

Low serum osmolality
Inappropriately concentrated urine – Urine osmolality >100 Urine Na >20
Clinical euvolaemia
Not on diuretics
Diagnosis of elimination – normal renal, thyroid, adrenal function

Question 22

SIADH management

Answer 22

Fluid restrict <800ml/day. PO sodium chloride, may give furosemide, Demeclocycline induces diabetes insipidus (reversing ADH effect), alternatively Tolvaptan

Question 23

Hypervolaemic hyponatraemia

Answer 23

CCF, Nephrotic syndrome, Liver cirrhosis

Treatment – fluid restrict and consider furosemide

Question 24

Correcting hyponatraemia too quickly

Answer 24

Too rapid correction of chronic hyponatraemia leads to central pontine/osmotic myelinosis. Aim to correct <12 mmol/L/day

Question 25

Treatment of hyponatraemia - acute

Answer 25

(tends to be iatrogenic, polydipsia, colonoscopy prep, ecstasy) If acute hyponatraemia (within 48 hours) and symptomatic – Give 3% hypertonic saline IV boluses +/- Furosemide

Question 26

Treatment of hyponatraemia - chronic

Answer 26

If chronic (>48 hours) and symptomatic – hypertonic saline boluses if having seizures. Otherwise isotonic saline and furosemide – aim to correct 8mmol/L in 24 hours If chronic and asymptomatic – water restriction, stop offending drug, if dehydrated – restore volume, if overloaded – Na and water restriction and diuretics

Question 27

Hyperkalaemia | Causes

Answer 27

 CKD, K rich diet with CKD (dried fruit, potatoes, oranges, tomatoes, avocados, nuts)  Drugs (ACEi/ARBs/Spironolactone/Amiloride/NSAIDs/ Heparin/ LMWH/Cyclosporin or calcineurin inhibitors/High dose Trimethoprim/ Digoxin toxicity/B- blockers)  Hypoaldosteronism (T4RTA), Addison’s disease, Acidosis, DKA (insulin deficiency), Rhabdomyolysis, tumour lysis, Massive haemolysis, Succinylcholine use  Rarer – Hyperkalaemic periodic paralysis, Gordon’s syndrome  Artifact Hyperkalaemia – haemolysis, leucocytosis, thrombocytosis

Question 28

Hyperkalaemia | Hyporeninaemic hypoaldosteronism

Answer 28

``` Hyporeninaemic Hypoaldosteronism (Type IV RTA) Hypochloraemic acidosis in about 50%, hyperkalaemia, typically with increased age and reduced eGFR classically in diabetes nephropathy, acute GN (nephritis), TIN/sickle cell, NSAIDs, CNIs, lupus nephritis ```

Question 29

Hyperkalaemia | Hypertensive with increased ECF

Answer 29

Often hypertensive with increased extra-cellular fluid volume (renin often down-regulated by fluid overload) Treat – low K diet, loop diuretic if overloaded

Question 30

Hyperkalaemia | ECG changes

Answer 30

```  Tented T waves  Prolonged QRS  Slurring of ST segment  Loss of P waves  Asystole ```

Question 31

Treatment of hyperkalaemia

Answer 31

1. Stabilizing the myocardium to prevent arrhythmias  10mls of 10% Calcium Gluconate over 5-10 minutes 2. Shifting potassium back into the intracellular space IV fast acting insulin (actrapid)  10 units and IV glucose/dextrose 50% 50mls Sodium Bicarbonate  500mls of 1.4% Sodium Bicarbonate  Only effective at driving Potassium intracellullarly if the patient is acidotic Salbutamol  5-10mg via nebulizer 3. Eliminating Potassium From the Body Calcium Resonium  15-45g orally or rectally, mixed with sorbitol or lactulose Frusemide  20-80mg depending on hydration status Dialysis  If resistant to medical treatment

Question 32

Hypokalaemia | Symptoms

Answer 32

Fatigue, constipation, proximal muscle weakness, paralysis, cardiac arrhythmias, worsened glucose control in diabetics, hypertension

Question 33

Hypokalaemia | Causes

Answer 33

 Pseudohypokalaemia – acute leukaemia  Extra-renal losses - Inadequate PO intake, Gut losses (vomiting, NG losses, secretory Diarrhoea, laxatives, VIPoma, Zollinger-Ellison, Ileostomy, enteric fistula)  Redistribution – Delirium tremens, beta agonists, insulin, caffeine, theophylline, alpha-blockers (Doxazosin), hypokalaemic periodic paralysis (inherited or acquired from thyrotoxicosis – Asian males)  Refeeding syndrome, alkalosis, vigorous exercise, glue-sniffing (Toluene can cause Fanconi/RTA II with renal potassium wasting)  Primary hyperaldosteronism (conn’s syndrome) Cushing’s syndrome, Secondary hyperaldosteronism (liver failure, heart failure, nephritic syndrome),  Renal losses (diuretics, RTA, Tubulopathies - Bartters/Liddles/Gittelmans), liquorice, glucocorticoids, hypomagnesaemia.

Question 34

Hypokalaemia | ECG changes

Answer 34

 Small T waves  U wave (after T)  Increased PR interval

Question 35

Hypokalaemia | Treatment

Answer 35

 Replace magnesium  Oral K replacement  IV K replacement (Usually in 0.9% NaCl - avoid in dextrose as induces further hypokalaemia)