Renal

Question 1

What are the normal ranges for electrolytes in the body?

Answer 1

• Sodium (Na⁺) 135-145 mmol/L
• Potassium (K⁺) 3.5-5 mmol/L
• Chloride (Cl^-) 95-105 mmol/L
• Bicarbonate (HCO₃^-) 24-30 mmol/L

Question 2

Describe some common principles related to sodium homeoostasis?

Answer 2

• hyponatraemia and hypernatraemia are disorders of water balance
  
  • hyponatraemia usually suggests too much water in the ECF relative to Na⁺
  • hypernatraemia usually suggests too little water in the ECF relative to Na⁺
• solutes (such as Na⁺, K⁺, glucose) that cannot freely traverse the plasma membrane contribute to effective osmolality and induce transcellular shifts of water
  
  • water moves out of cells in response to increased ECF osmolality
  • water moves into cells in response to decreased ECF osmolality
• ECF volume is determined by Na⁺ content rather than concentration
  
  • Na⁺ deficiency leads to ECF volume contraction
  • Na⁺ excess leads to ECF volume expansion
• clinical signs and symptoms of hyponatremia and hypernatremia are secondary to cells (especially in the brain) shrinking (hypernatremia) or swelling (hyponatremia)

Question 3

How do you asses volume status on physical exam?

Answer 3

Question 4

Define hyponatraemia.

Answer 4

A serum sodium level of <130 mmol/L

Question 5

What are the different types of hyponatraemia and their causes?

Answer 5

• Factitious ‘pseudohyponatraemia’
  
  • associated with hyperglycaemia, hyperlipidaemia, hyperproteinaemia
  • correct the sodium for hyperglycaemia by adjusting hte serum sodium up by 1 mmol/L for every 3 mmol/L elevation in blood sugar.
• Hypovolaemic hyponatraemia
  
  • urinary sodium >20 mmol/L: renal cuases include diuretics, Addison’s disease, salt-losing nephropathy, glycosuria, ketonuria.
  • Urinary sodium <20mmol/L; extrarenal losses such as vomiting, diarrhoea, burns, pancreatitis.
• Normovolaemic hyponatraemia
  
  • Urine osmolality > serum osmolality:
    
    • syndrome of inappropriate antidiuretic hormone secretion (SIADH) due to head injury, meningoencephalitits, CVA, pneumonia, COPD, neoplasia, HIV, drugs such as carbamazepine, NSAIDs and antidepressants such as SSRIs
    • Positive-pressure ventilation, porphyria
  • Urine osmolality < serum osmolality:
    
    • hypotonic post-operative fluids such as 5% dextrose or 4% dextrose 1/5 normal saline, TURP irrigation fluid, psychogenic polydipsia, ‘tea and toast’ diet, beer potomania.
• Hypervolaemic hyponatraemia
  
  • Urinary sodium <20 mmol/L: congestive cardiac failure, cirrhosis, nephrotic syndrome, hypoalbuminaemia, hepatorenal syndrome
  • Urinary sodium >20 mmol/L: steroids, cerebral salt wasting, chronic renal failure, hypothyroidism.

Question 6

What are the clinical features of hyponatraemia?

Answer 6

Clinical features progress as the serum sodium level drop, but depend also on the rate of fall, i.e. the more rapid the fall the greater the symtpoms:

• Na > 125 mmol/L: usually symptomatic
• Na 115-125 mmol/L: lethargy, weakness, ataxia, and vomiting
• Na <115 mmol/L: confusion, headache, convulsions, and coma

Question 7

What are the complications of hyponatraemia?

Answer 7

• Seizure, coma, respiratory arrest, permanent braine damage, brainstem herniation, death
• risk of brain cell shrinkage with rapid correction of hyponatraemia
  
  • can develop osmotic demyelination of pontine and extrapontine neurons; may be irreversible (e.g. central pontine myelinolysis: cranial nerve palsies, quadriplegia, decreased LOC)

Question 8

First thought Central pontine myelinolysis.

Answer 8

• Cranial nerve palsies
• Quadriplegia
• Decreased LOC

Question 9

What are the risk factors for developing osmotic demyelination?

Answer 9

• rise in serum [Na⁺] with correction >8 mEq/L/d if chronic hyponatremia
• associated hypokalemia
• if patient with hyponatremia and hypovolemia is given large volume of isotonic fluid (ADH is stimulated by hypovolemia; when hypovolemia is corrected, the ADH level falls suddenly causing sudden brisk water diuresis, and therefore rapid rise in serum Na⁺ level)

Question 10

What Ix need to be order for someone with hyponatraemia?

Answer 10

• Bloods: FBC, LFTs, UECs, glucose, serum osmolality, TSH, free T4, cortisol levels
• Urine: osmolality, urine Na⁺ <10-20 mEq/L suggests volume depletion as the cause of hyponatremia)
• assess for causes of SIADH
• ECG
• consider CXR and possibly CT chest if suspect pulmonary cause of SIADH (e.g. small cell lung cancer)
• consider CT head if suspect CNS cause

Question 11

What is the management of hyponatraemia?

General measures for all patients

Answer 11

• Commence high-flow oxygen via face mask
• Discontinue implicated drug therapy and treat the underlying medical condition, e.g. antibiotics for sepsis, treat pain, nausea etc.
• Restrict free water intact - to 50% of estimated maintenance fluid requirements in SIADH, i.e. around 750ml/day
• promote free water loss
• Aim to increase the serum Na⁺ gradually by 0.5 mmol/L per h, to a max rate of 12 mmol/L per 24 h.
• Carefully monitor serum Na+, urine volume and urine tonicity (e.g. high output of dilute urine may be a sign of impending rapid serum sodium correction)

Question 12

What is the management of hyponatraemia?

Definietly acute (known to have developed over <24-48h)

Answer 12

• commonly occurs in hospital (dilute IV fluid, post-operative increased ADH)
• less risk from rapid correction since adaptation has not fully occurred
• if symptomatic
  
  • correct rapidly with 3% NaCl 1-2 ml/kg/h up to serum [Na⁺] = 125-130 mmol/L
  • may need furosemide to address volume overload
• if asymptomatic, treatment depends on severity
  
  • if marked fall in plasma [Na⁺], treat as symptomatic

Question 13

What is the management of hyponatraemia?

Chronic or unknown

Answer 13

• GET SENIOR DOCTOR HELP - especially if neuro symptoms
• if severe symptoms (seizures or decreased LOC)
  
  • must partially correct acutely
  • aim for increase of Na⁺ by 1-2 mmol/L/h for 4-6 h
  • limit total rise to 8 mmol/L in 24 h
  • IV 3% NaCl at 1-2 ml/kg/h
  • may need furosemide
• if asymptomatic
  
  • water restrict to <1 L/d fluid intake
  • consider IV 0.9% NS + furosemide (reduces urine osmolality, augments excretion of H 2 O)
  • consider NaCl tablet
• refractory
  
  • furosemide and oral salt tablets
  • oral urea (osmotic aquaresis)
  • V2 receptor antagonists (e.g. tolvaptan)
• always pay attention to patient’s ECF volume status – if already volume-expanded, unlikely to give NaCl; if already volume-depleted, almost never appropriate to give furosemide

Question 14

What is syndrome of inappropriate antidiuretic hormone (SIADH) secretion and what are some of the causes?

Answer 14

1. urine that is inappropriately concentrated for the serum osmolality
2. high urine sodium (>20-40 mmol/L)
3. high FE_Na

Question 15

Define hypernatraemia?

Answer 15

• hypernatremia: serum [Na⁺] >145 mmol/L
• too little water relative to total body Na⁺; always a hyperosmolar state
• usually due to NET water loss, rarely due to hypertonic Na⁺ gain
• less common than hyponatremia because patients are protected against hypernatremia by thirst and release of ADH

Question 16

What are the causes of hypernatraemia?

Answer 16

• Decreased fluid intake with normal fluid loss:
  
  • disordered thirst perception e.g. hypothalamic lesion
  • inability to communicate water needs, e.g. cerebrovascular accident, infants, elder (dementia, swallowing difficulties, stroke, bed-bound), coma, surgical, intubated pts.
• Hypotonic fluid loss, with water loss in excess of salt loss
  
  • skin loss from excessive sweating in hot climates, dermal burns
  • gastrointestinal loss from diarrhoea or vomiting
  • renal loss from impaired salt-concentrating ability, e.g. diabetes insipidious, osmotic diuretic agents, hyperglycarmia, hypercalcaemia, chronic renal disease.
• Increased salt load:
  
  • hyperaldosteronism or Cushing’s syndrome
  • ingestion of sewater, salt tablets, and administration of sodium bicarbonate or hypertonic saline

Question 17

What are the signs and symptoms of hypernatraemia?

Answer 17

Signs and symptoms of hypernatraemia are progressive and directly related to theserum osmolality level. Look for:

• Increased thirst, weakness, lethargy and irritability (>375 mOsm/kg)
• Altered mental status, ataxia, tremors and focal neurological signs (>400 mOsm/kg)
• Seizures and coma (>430 mOsm/kg)

Question 18

What are the complications of hypernatraemia?

Answer 18

• Increased risk of vascular rupture resulting in intracrranial haemorrhage
• rapid correction may lead to cerebral aedema due to congoing bran hyperosmolality.

Question 19

What Ix used to assess hypernatraemia?

Answer 19

• Blood: FBC, UECs, LFTs and serum osmolality
• ECG and CXR

Question 20

How is hypernatraemic Tx?

Answer 20

• Give high flow-oxygen via face mask
• general measures for all patients
  
  • give free water (oral or IV)
  • treat underlying cause
  • monitor serum Na⁺ frequently to ensure correction is not occurring too rapidly
• if evidence of haemodynamic instability, must first correct volume depletion with NS bolus
• loss of water is often accompanied by loss of Na⁺ , but a proportionately larger water loss
• use formula to calculate free water H₂O deficit and replace
• encourage patient to drink pure water, as oral route is preferred for fluid administration
• if unable to replace PO or NG, correct H₂O deficit with hypotonic IV solution (IV D5W, 0.45% NS [half normal saline], or 3.3% dextrose with 0.3% NaCl [“2/3 and 1/3”])
• use formula to estimate expected change in serum Na⁺ with 1 L infusate
• aim to to lower [Na⁺] by no more than 12 mmol/L in 24 h (0.5 mmol/L/h)
• must also provide maintenance fluids and replace ongoing losses
• general rule: give 2 ml/kg/h of free water to correct serum [Na⁺] by about 0.5 mmol/L/h or 12 mmol/L/d

Question 21

Define diabetes insipidus.

Answer 21

• collecting tubule is impermeable to water due to absence of ADH or impaired response to ADH
• defect in central release of ADH (central DI) or renal response to ADH (nephrogenic DI)

Question 22

Describe the aetiology of diabetes insipidus?

Answer 22

• central DI: neurosurgery, granulomatous diseases, trauma, vascular events, and malignancy
• nephrogenic DI: lithium (most common), hypokalemia, hypercalcemia, and congenital

Question 23

How is diabetes insipidus diagnosed?

Answer 23

• Monitor: urine volume
• Bloods:
  
  • Urine osmolality, urine sodium
  • Antidiuretic hormone
  • UEC
• Water depreivation test - definitive diagnosis

Question 24

Describe common principles that apply to potassium homeostasis.

Answer 24

• approximately 98% of total body K⁺ stores are intracellular
• normal serum K⁺ ranges from 3.5-5.0 mmol/L
• in response to K⁺ load, rapid removal from ECF is necessary to prevent life-threatening hyperkalemia
• insulin, catecholamines, and acid-base status influence K⁺ movement into cells
  
  • aldosterone has a minor effect
• potassium excretion is regulated at the distal nephron
  
  • K⁺ excretion = urine flow rate x urine [K⁺]

Question 25

What are some factors that increase renal K⁺ loss?

Answer 25

• hyperkalemia
• increased distal tubular urine flow rate and Na⁺ delivery (thiazides and loop diuretics)
• increased aldosterone activates epithelial sodium channel in cortical collecting duct, causing Na⁺ reabsorption and K⁺ excretion
• metabolic alkalosis
• hypomagnesemia
• increased non-reabsorbable anions in tubule lumen: HCO₃^–, penicillin, salicylate

Question 26

What are the causes of hypokalaemia?

Answer 26

• Inadequate intake of K+, e.g. alcoholism, starvation
• Abnormal gastrointestinal losses from vomiting, diarrhoea and laxative abuse
• Abnormal renal losses:
  
  • Cushing’s, Conn’s and Bartter’s syndrome
  • ectopic adrenocortiotrophic hormone (ACTH) production
  • drugs, e.g. diuretics and steroids
  • hypomagnesaemia
• Compartmental shift:
  
  • metabolic alkalosis
  • insulin
  • drugs, e.g. salbutamol, terbutaline, aminophylline
  • hypomagnesaemia

Question 27

What are the signs and symptoms of hypokalaemia?

Answer 27

• MIld 3-3.5 mmol/L: asyptomatic
  
  • N/V, fatigue, generalised weakness, myalgia, muscle cramps, and cnstipation
• Severe: arrhythmias, muscle necrosis, and rarely parralysis with eventual respiratory impairment
• Arrhythmias occur at variable levels of K+; more likely if digoxin use, hypomagnesaemia or CAD

Question 28

What are the ECG changes that are seen in hypokalaemia?

Answer 28

• Flat or inverted T waves, prominent U waves
• Prolonged Q-T interval
• ST segment depression
• With severe hypokalaemia: PR prolongation, wide QRS, ventricular arrhythmias, including torsade de points

Question 29

What is your approach to a pt with hypokalaemia?

Answer 29

• Emergency measures: obtain ECG; if potentially life threatening, begin treatment immediately
• rule out transcellular shifts of K⁺ as cause of hypokalaemia
• Assess contribution of dietary K⁺ intake
• Spot urine K:Cr (should be less than 1 in setting of hypokalaemia
  
  • if <1 consider GI loss
  • if >1 consider a renal loss
• consider 24h K⁺ excretion
• if renal K⁺ loss, check BP and acid-base status
• may also assess plasma renin and aldosterone levels, serum [Mg²⁺]

Question 30

Describe the treatment of hypokalaemia.

Answer 30

• Treat underlying cause
• Replace K⁺ immediately in the following situtations
  
  • Serum K⁺ <3.0mmol/L
  • Serum K⁺ 3.0-3.5 mmol/L in patients with chronic heart failure or cardiac arrhythmias, particularly if on digoxin or following myocardial infarction.
• Give KCl 20-40 mmol/h i.v under ECG control using a fluid infusion device, but do not exceed 40mmol/h in peripheral line
  
  • rate of Kinfusion should not exceed 10 mmol/hour
• Can use K+ sparing drugs:
  
  • spironolactone 50-100 mg PO OR amiloride 5 mg PO
• Risk of hyperkalaemia with K⁺ replacement especially high in elderly, diabetes and patients with decreased renal function

Question 31

What are the signs and symptoms of hyperkalaemia?

Answer 31

• Usually asymptomatic but may develop nauseea, palpitations, muscle weakness, muscle stiffness, paresthesias, areflexia, ascending paralysis, and hypoventilation
• Impaired renal ammoniagenesis and metabolic acidosis

Question 32

What are the ECG changes that occur in hyperkalaemia?

Answer 32

• ECG changes and cardiotoxicity (do not correlate well with serum [K⁺])
• Tall, peaked (tented) and narrow T waves
• Prolonged PR interval with flattened P waves
• ST segment depression
• QRS widening, absent P waves and sinusoidal wave pattern
• Ventricular fibrillation, pulseless electrial activity (PEA) or asystole
• AV block

Question 33

What are the causes of hyperkalaemia?

Answer 33

• Increased K⁺ intake:
  
  • oral or i.v K⁺ supplements, transfusion of stored blood
• Increased production:
  
  • Burns, ischaemia, haemolysis
  • Rhabdomyolysis, tumour lysis syndrome
  • Intense physical activity
• Decreased renal excretion
  
  • acute of chronic renal failure
  • Drugs, e.g. K⁺-sapring diuretics, angiotensin-coverting enzyme (ACE) inhibitors, NSAIDs
  • Addison’s disease, hypoaldosteronism
• Transcellular compartmental shift
  
  • Acidosis (metabolic or respiratory)
  • hyperglycaemia
  • digoxin poisoning, suxamethonium
• Factitious
  
  • haemolysed specimen, thrombocytosis, massive leukocytosis

Question 34

What is your approach to a pt with hyperkalaemic?

Answer 34

1. emergency measures: obtain ECG, if life threatening begin treatment immediately
2. rule out factitious hyperkalemia; repeat blood test
3. hold exogenous K⁺ (PO and IV) and any K⁺ retaining medications
4. assess potential causes of transcellular shift
5. estimate GFR (calculate CrCl using Cockcroft-Gault)

Question 35

What is the management of hyperkalaemia?

Answer 35

• Give high-flow 0₂ via face-mask and cease any exogenous K⁺ supplementation
• Severe hyperkalaemia (>6.5 mmol/L) or hyperkalaemia with life-threatening ECG changes. Provide immediate cardioprotection to prevent cardiac arrest:
  
  • Give 10% CaCl₂ 10ml i.v over 2-5 min, repeated until the ECG and cardiac output normalises
    
    • this does not lower the K⁺, but antagonises the deleterious effects of hyperkalaemia on the myocardium, reducing the risk of ventricluar fibrillation (onset of protection in 1-3 mins)
  • Use the other therapies outlined to shift K⁺ into the cells and eliminate K⁺ from the body.
• Moderate hyperkalaemia (6.0-6.5 mmol/L)
  
  • shift K⁺ intracellularly with:
    
    • 50% dextrose 50 ml i.v with 10 units of soluble insulin over 20 mins (onset of action 15 min, with maximal effect within 1 h)
      
      • Beware more rapid delivery of the 50% dextrose with the insulin as it may paradoxically release intracellular K⁺ due to its hypertonicity.
      • Give the soluble insulin alone in hyperglycaemic patients with blood sugar of >12 mmol/L (i.e without dextrose)
    • Salbutamol 10-20 mg nebulised. Several doses may be required (onset of action 15 min)
    • 8.4%sodium bicarbonate 50 ml i.v over 5 min, provided ther is no danger of fluid overload, as it contains 50 mmol sodium
      
      • less effective as a sole agent, but works well in combination wtih salbutamol and dextrose/insulin (onset of action 15-30 min), and if a metabolic acidosis is present.
• Mild hyperkalaemia
  
  • remove K⁺ from the body with
    
    • Frusemide (furosemide) 40-80 mg i.v (onset of action with diuresis, provided not anuric)
    • K⁺-exchange resin: calcium resonium 30g orally or by enema (onset of action 1-3h after administration)
• refer the patient to the medical team, and according to the K⁺ level and underlying cause, organise haemodialysis or peritoneal dialysis as needed, particularly in known renal failure.

Question 36

Define acute kindney injury.

Answer 36

• abrupt decline in renal function leading to increased nitrogenous waste products normally excreted by the kidney
• formerly known as Acute Renal Failure

Question 37

What are the clinical features of AKI?

Answer 37

• azotemia (increased BUN, Cr)
• abnormal urine volume: formally <0.5 ml/kg/h for >6 h but can manifest as anuria, oliguria, or polyuria

Question 38

What is the criteria used to diagnose and stage AKI?

Answer 38

• RIFLE criteria
  
  • Risk: serum creatinine ↑ x 1.5; or urine production <0.5 ml/kg per hour for 6h
  • Injury: serum creatinine ↑ x 2; or urine production <0.5ml/kg per hour for 12 h
  • Failure: serum creatinine ↑ x 3 or >355 µmol/L (with acute rise >44); or urine output <0.3 ml/kg per hour for 24h ‘oliguria’, or anuria for 12h
  • Loss: peristent AKI with complete loss of kidney function for >4 weeks
  • End-stage kidney disease: complete loss of kidney function for >3 months.

Question 39

What are the causes of AKI?

Answer 39

• Pre-renal failure: (decreased rneal perfusion)
  
  • shock, burns, sepsis, dehydration, low-output cardiac failure
  • renovascualr disease: renal stenosis, renal artery emboli
• Intrinsic renal failure:
  
  • acute tubular necrosis (ATN): following prolonged pre-renal hypoperfusion, ischaemia, sepsis, toxins, e.g. gentamicin, radiographic contrast, myoglobin, ethylene glycol
  • acute interstitial nephritis: drugs (including Abx and NSAIDs), infection, sarcoidosis, autoimmune disease, e.g. SLE
  • acute glomerulonephritis: post-infectious, vasculitis, autoimmune disease, complement-related
  • acute cortical necrosis: profound hypoperfusion, e.g. obstetric complication with haemorrhage
  • Miscellaneous: ACE inhibitor, thrombotic microangiopathy. malignant hypertensiion, renal vein thrombosis
• Post renal failure: Obstruction may be extranural, intramural or intraluminal at any point from the renal tubule to the distal urethra. Causes include:
  
  • ureteric obstruction to a single kidney, or bilateral ureteric obstruction to both kidneys
  • retroperitoneal fibrosis; ureteric strictures, calculi or crystal deposition; tumours such as uteric cancer; prostatic disease such as BPH or malignancy

Question 40

On examination of a patient with AKI what should you look for?

Answer 40

• Volume status:
  
  • signs of volume depletion: hypotension, tachycardia, decreased skin tugor, dry mucous membranes in a pt with decreased renal perfusion associated with a pre-renal condition.
  • signs of volume overload: raised JVP, peripheral oedema and respiratory crepitations in intrinsic renal disease.
• Clinical manifestations of acute uraemia: sallow complexion, asterixis (flap), pericardial or pleural rub, pulmonary oedema or pleural effusion, altered mental status, confusion, seizures
• Signs of post-renal obstruction: enlarged prostate on PR exam, cervical or uterine mass lesion on vaginal exam, and an enlarged palpable bladder.

Question 41

What is the approch in terms of Ix for AKI?

Answer 41

• IV cannula and ECG - hyperkalaemia, AF causing renal embolic disease
• Bloods: FBC, UEC, LFTs, blodd sugar, CK, calcium and uric acid
• ABG or VBG
• Urine (midstream): MCS, sediments, casts and crystals, osmolarity and electrolytes
• Bladder scan - post-renal causes
• Insert IDC
• CXR: volume overload, metastatic disease, pulmonary-renal syndrome such as Wegener’s granulomatosis
• US abdo - kidneys, ureter and bladder (assess kidney size, hydronephrosis, psotrenal obstruction)
• Renal biopsy - diagnosis uncertain, prerenal azotaemia or ATN is unlikely, oliguria persists >4wks

Question 42

What is the treatment of AKI?

Answer 42

• preliminary measures
  
  • prerenal
    
    • correct prerenal factors: optimize volume status and cardiac performance using fluids that will stay in the plasma subcompartment (NS, albumin, blood/plasma), hold ACEI/ARB (gently rehydrate when needed, e.g. CHF)
  • renal
    
    • address reversible renal causes: discontinue nephrotoxic drugs, treat infection, and optimize electrolytes
  • postrenal
    
    • consider obstruction: structural (stones, strictures) vs. functional (neuropathy)
    • treat with Foley catheter, indwelling bladder catheter, nephrostomy, stenting
• treat complications
  
  • fluid overload
    
    • NaCl restriction
    • high dose loop diuretics
  • hyperkalemia
    
    • adjust dosages of medications cleared by kidney (e.g. amiodarone, digoxin, cyclosporin, tacrolimus, some antibiotics, and chemotherapeutic agents)
    • dialysis
• definitive therapy depends on aetiology

note: renal transplant is not a therapy for AKI

Question 43

What is the triple whammy?

Answer 43

• Diuretics
• NSAIDs
• ACEI/ARBs

Question 44

What are the indications for dialysis?

Answer 44

Refractory to medical therapy - AEIOU

• Acidosis
• Electrolyte imbalance (K⁺)
• Intoxication (lithium)
• Overload (fluid)
• Uraemic encephalopathy, pericarditis, urea >35-50 mM

Question 45

Define chronic kidney disease, the markers for and clinical of chronic kidney disease?

Answer 45

• progressive and irreversible loss of kidney function
• abnormal markers (Cr, urea)
  
  • GFR <60 mL/min for >3 mo; or
  • kidney pathology seen on biopsy; or
  • decreased renal size on U/S (kidneys <9 cm)
• clinical features of CKD
  
  • volume overload and HTN
  • electrolyte and acid-base balance disorders (e.g. metabolic acidosis)
  • uraemia

Question 46

What are the causes of chronic kidney disease?

Answer 46

• DM 42.9%
• HTN 26.4%
• Glomerulonephritis 9.9%
• Other/Unknown 7.7%
• Interstitial nephritis/ Pyelonephritis 4.0%
• Cystic/Hereditary/Congenital 3.1%
• Secondary GN/Vasculitis 2.4%

Question 47

What is the management of chronic kidney disease?

Answer 47

• diet
  
  • preventing HTN and volume overload
    
    • Na+ and water restriction
  • preventing electrolyte imbalances
    
    • K⁺ restriction (40 mEq/d)
    • PO₄^3- restriction (1 g/d)
    • avoid extra-dietary Mg₂⁺ (e.g. antacids)
  • preventing uremia and potentially delaying decline in GFR
    
    • protein restriction with adequate caloric intake in order to limit endogenous protein catabolism
• medical
  
  • adjust dosages of renally excreted medications
  • HTN: ACEI (target 130/80 or less), loop diuretics when GFR <25 mL/min
  • dyslipidemia: statins
  • calcium and phosphate disorders:
    
    • calcium supplements treats hypocalcemia when given between meals and binds phosphate when given with meals
    • consider calcitriol (1,25-dihydroxy-vitamin D) if hypocalcemic
    • sevelamer (phosphate binder) if both hypercalcemic and hyperphosphatemic
    • vitamin D analogues are being introduced in the near future
    • cinacalcet for hyperparathyroidism (sensitizes parathyroid to Ca²⁺, decreasing PTH)
  • metabolic acidosis: sodium bicarbonate
  • anemia: erythropoietin injections (Hct <30%); target Hct 33-36%
  • clotting abnormalities: DDAVP if patient has clinical bleeding or invasive procedures (acts to reverse platelet dysfunction)
• dialysis (hemodialysis, peritoneal dialysis)
• renal transplantation

Question 48

What are the indications for dialysis?

Answer 48

Question 49

Describe what is absorbed and secreted in the kidneys and where and which hormones act on which areas of the kidney.

HINT: best to draw out a tubule

Answer 49