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Management overview

1. Diet: Protein restriction with adequate calories K+ restriction Na and water restriction Phosphate restriction Avoid extra-dietary magnesium (antacids)

2. Medical: Treat secondary hyperPTH Calcium supplements Calcitriol Phosphate binder Vitamin D analogues Cinacalcet for hyperparathyroidism (sensitizes parathyroid to Ca2+, decreasing PTH) Sodium bicarbonate EPO ejections ACEi Statins Adjust medications Stop nephrotoxic medications. Statin therapy. Optimise diabetes management.

3. Dialysis

4. Renal translpant


Prevention of progression

1. As management 2. Control HTN, DM, smoking cessation, physical activity, weight loss 3. Avoid neprhotoxins 4. Address reversible causes of AKI


Presentation of renal failure

1. Volume overload 2. Electrolyte abnormalities 3. Uremic syndrome


Complications of renal failure


• CNS: decreased LOC, stupor, seizure

• CVS: cardiomyopathy, CHF, arrhythmia, pericarditis, atherosclerosis

• GI: peptic ulcer disease, gastroduodenitis, AVM

• hematologic: anemia, bleeding tendency (platelet dysfunction), infections

• endocrine: ƒƒdecreased testosterone, estrogen, progesterone ƒƒ increased FSH, LH

• metabolic: ƒƒ renal osteodystrophy: secondary increased PTH due to decreased Ca2+, high PO4 3- and low active vitamin D ŠŠosteitis fibrosa cystica, ƒƒhypertriglyceridemia, accelerated atherogenesis, ƒƒdecreased insulin requirements, increased insulin resistance

• dermatologic: pruritus, ecchymosis, hematoma, calciphylaxis (vascular Ca2+ deposition)


Indications for dialysis


Hyperkalemia (refractory)

Acidosis (refractory)

Volume overload (refractory)

Elevated urea (>35-50 mM)



Edema (pulmonary)


Number of people on RRT, number at risk of CKD, number of people with CKD

1. 1 in 1500 on RRT

2. 1 in 9 CKD

3. 1 in 3 at risk of CKD


Risk factors

1.  >60


3. Diabetes

4. CVD

5. hypertension

6. smoking, 

7. diabetes FHx,

8. obesity-->screen in adults >35 with


Screening for CKD in ATSI

1. Screen for risk factors annually in 18-29 yo

2. All >30, 18-29 w/ risk factor: urine ACR, eGFR, BP every 1-2 years


Systemic manifestations

1. Fluids and electrolytes: +K, deH, edema, metabolic acidosis, +Urea/Creatinine

2. Calcium, Phosphate and bone: renal osteodystrophy, secondary hyperPTH, hypocalcemia (-ve conversion vit D, -ve absorption in GIT, acidosis), hyperphosphatemia

3. Sexual dysfunction

4. Hematological: anemia (-ve EPO, blood loss due to defective PLTs), hemolytic

5. Cardiopulmonary: Pulmonary edema, cardiomyopathy, pericarditis, HTN

6. GIT: NVD, esophagitis, gastritic, colitis

7. Neuromuscular: myopathy, peripheral neuropathy, encephalopathy

8. Dermatologic: Sallow colour, dermatitis, pruritis, nodules


Renal replacement therapy in acute setting indications

1. Metabolic acidosis

2. +K >6 despite other management

3. +plasma urea and creatinine
> 30 mmol/L  (180 mg/dL) and creatinine
> 600 μmol/L (6.8 mg/dL)

4. Fluid overload w/ complications->pulmonary edema, heart failure

5. Uremic pericarditis/encephalopathy

Hemofiltration or hemodialysis


Renal replacement therapy chronic: reasons for one over the other

1. Hemodialysis: more hemodynamically stable, more time consuming, must be in hospital, time away. Needs increased compliance with diet and fluids.

Risks: hemodynamic instability, bleeding, sepsis, hypersensitivity, air embolus, arrythmias

2. Peritoneal: more comfort, in own home, diet less restrictive. May not have suitable living, not stable household, non compliance, infection risk


Complications and associated management: HTN, bone, albuminuria, glycemic control, anemia

1. HTN: a) Lifestyle b) ACEi first line, aim <130/80 in diabetic, 140/90 in others. Monitor eGFR/K. Cease if eGFR drop >25% in 2 months and reconsider/refer. If K 6-6.5 lower, K wasting diuretic, K diet restricting. If then X<6->stop and consider BB, CCB, thiazide. >6.5= emergency

2. Bone: Keep Phosphate and Ca in normal range, PTH 2-9 X upper limit, vitamin D. 

Phosphate diet restriction (get dietician help)-> cheese, milk, eggs, use phosphate binders (Calcium carbonate)

Consider calcitriol in later stages.

If phosphate controlled, calcium leves usually improve. 

3. Albuminuria: ACEi, ARB, reduce salt, use spirinolactone cautiously

4. Glycemic: Pre-prandial BSL 4.0-6.0 mmol/L
HbA1c <7.0%/53mmol/mol

Hypoglycemics, diet, insulin, incretins, gliptins

5. Anemia: 
Hb 100 – 115 g/L
Prior to commencement of epoetin: Ferritin > 100 μg/L
TSAT >20%
Once epoetin commenced: Ferritin 200-500 μg/L
TSAT 30-40%

Need neprhologist.

Iron supplement

Rule out other causes->Vit B12, folate, TSH


Mangement of complications: uremia, restless leg, hyperkalemia, sleep apnea, depression, acidosis

1. Uremia

Dialysis when urea ++

Low protein diet, fluid control

Antiemetics have limited value

2. Restless leg

Iron supplementation, baths and massages, compresses, levodopa, benzodiazepines

3. Hyperkalemia

Low K diet, correct acidosis, K wasting diuretics, resonium A powder, cease ACEi/ARB/Spirinolacton if >6.

4. Acidosis

?Sodium bicarbonate

5. Sleep apnea

Weight loss

Avoid CNS depressants


6. Depression

Psychosocial intervention

Antidepressants at low dose


Medications in CKD: drugs needing reduction, affects on kidney

1. Dose reduction

Benzodiazepines, gabapentin, lithium
Exenatide, insuin, metformin
Sotolol, spirinolactone

Opioid analgesics
Digoxin, fenofibrate
Saxagliptin (DPP-4 inibitors)

2. Adverse effects


NSAIDs, COX 2 i, ACE, diuretics->tripple whammy






1. eGFR <60 w/o signs of kidney disease or evidence of kidney damage-> albuminuria, hematuria, structural, pathalogical

2. Present for >3 months


Screening test for CKD

1. urinary ACR measurement  in a first void spot specimen=
best measure for albuminuria,.not possible: can use
random spot test--> repeat to confirm persistence

2. if abnormal need 2 of 3 abnormal readings over 3 months


DIfferential for +ACR

UTI- dipstick, Acute febrile illness - T
+Dietary protein- Hx, ++exercise last
24 hours- Hx
Mensturation/vaginal discharge- Hx
NSAIDS- Hx, Congestive, cardiac failure


Is eGFR clinically reliable

1. No, dependent on age

2. +muscle under, -ve muscle over

3. +Protein, vegetarian, creatine supplements interfere

4. Extremes of body size


If abnormal eGFR

1. Urine ACR

2. eLFTs

3. Serum creatinine

4. FBC

5. Lipids, glucose

6. Urine MCS

7. Refer to neprhologist when GFR <30, drop in baseline 60
by >5 over 6 months confirmed by 3 readings
Glomerular hematuria w/ macroA
CKD + HTN not ocntrolled despite  three antihypertensive 


Management action plans: yellow, orange, red

1. Yellow >60 w/ microA, >40-59 

Annual review:

a) exclude treatable, adress CVD, avoid nephrotoxic drugs

b) BP, lifestyle

c) Urine ACR, UEC, BUN, eGFR, HbA1C, statins

2. Orange 30-60 w/ micro >30-44

3-6 monthly

a) Same as yellow + detect complications, adjust medication doses, refer when indicated

b) +FBC, CMP, PTH when <45   + Urine ACR, UEC, BUN, eGFR, HbA1C, statins

3. Red action plan

MacroA, eGFR <30

1-3 monthly review

a) Same goals, + referall + prepare for dialysis + AHD

b) Same investigations + edema, +advanced care planning



Stage 1: kidney damage with normal or increased GFR, ≥90 mL/minute/1.73m^2

Stage 2: kidney damage with mild decrease in GFR, 60 to 89 mL/minute/1.73m^2

Stage 3a: kidney damage with moderate decrease in GFR, 45 to 59 mL/minute/1.73m^2

Stage 3b: kidney damage with moderate decrease in GFR, 30 to 44 mL/minute/1.73m^2

Stage 4: kidney damage with severe decrease in GFR, 15 to 29 mL/minute/1.73m^2

Stage 5: kidney failure (end-stage kidney disease), with GFR <15 mL/minute/1.73m^2


Define acute renal failure

Acute kidney injury is defined by a rise in the serum creatinine of ≥23 micromol/L (≥0.3 mg/dL) from baseline, a 50% increase in serum creatinine from baseline, or a reduction in urine output of <0.5 mL/kg/hour for more than 6 hours that occurs over a period of days to weeks.


Counselling use of ACEi

1. Used to treat hypertension, block conversion of angiotensinogen to angiotensic 2, also inhibit bradykinin breakdown.

2. Avoid in pregnancy. 

3. Common adverse effects: hypotension, headache, dizziness and cough. Also hyperkalemia, fatigue, nausea, renal impairment

4. Infrequently cause rash, angioedema, diarrhea and elevated LFTs

5. Cough is a persistent, non-productive. Not dose dependent, unlikely to respond. Some may need to stop.

6. May feel dizzy, get up slowly

7. Do not take potassium supplements, unless required.

8. when starting an ACE inhibitor:

stop potassium supplements and potassium-sparing diuretics

in heart failure, consider reducing dose or withholding other diuretics for 24 hours before starting an ACE inhibitor

review use of NSAIDs (including selective COX‑2 inhibitors)

start with a low dose

check renal function and electrolytes before starting an ACE inhibitor and review after 1–2 weeks