CHRONIC KIDNEY DISEASE

DIAGNOSIS (NB!) | DEFINITION

1. Reduction in function
a. GFR < 60ml/min (normal is > 90) AND/OR
2. Kidney damage (symptoms)
a. Proteinuria (albuminuria)
3. + Health implications/complications
a. Abnormal structure (small kidneys, single kidney, polycystic kidney)
FOR > 3 MONTHS (specific health implications)
NB  Therefore can’t diagnose CKD on one visit, needs at least 3 months as majority of
acute renal injury is reversible
Cause of CKD is NB for treatment and prognosis

1. REDUCTION IN FUNCTION
 Reduced GFR
o 24 hour urine  Creatinine clearance (surrogate or substitute for GFR)  NB
o eGFR (estimated)
 Increased s-Creatinine
o In renal failure  s-Creatinine only increases when the GFR reduced by 50% (by the time
creatinine has gone up you have already lost half your function)
 Renal failure
 Rhabdomyolysis
 Large muscle mass
 Vegetarian diet, drugs (cimetidine gives false high)
 Increased s-Urea (NB)
o Renal failure
o ↑ protein load (eg. high protein diet, GI bleed)
o Urea = made in liver (low urea with liver disease)

2. KIDNEY DAMAGE
1. Albuminuria (repeat the measurement)
a. Urinary albumin/creatinine ratio (mmol/L)
i. > 30 = CKD
2. Microalbuminuria (detects early CKD) Albuminuria:
a. Dipstick (-) as it does not show up on dipstick
b. Urine albumin/creatinine ratio > 3.5 – 15 - normal = < 30
c. Only in diabetics (don’t need high BP) and hypertensives  - positive = 30 – 299
Put them on ARB or ACE
Proteinuria:
3. Proteinuria (macroalbuminuria)
a. Dipstick (+) – (3+) - normal = < 150
b. > 300mg/24H - mild = 150 – 490
c. Nephrotic range: > 3.5g/24H - severe = > 300
3. KIDNEY STRUCTURE (HEALTH IMPLICATION)

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 I. Renal size (U/S)
a. Small in CKD, except with:
i. DM! NB  Can still be normal
ii. PCKD
iii. Amyloidosis
iv. Myeloma
v. Hydronephrosis
b. Loss of cortico-medullary differentiation
i. Not clearly defined
II. Scars
III. Cysts
a. Simple
b. Polycystic (Autosomal Dominant)
IV. Large size  Hydronephrosis
a. Obstruction
NB  You need to do U/S of the kidneys when there is kidney damage!

SIGNS AND SYMPTOMS

 Symptoms
o Mostly asymptomatic or non-specific
 Signs
o Anaemia/Pallor
 Decreased erythropoietin (EPO)
o Bleeding tendency
 Excretion of Protein S & C (increased tendency to clot)
o Uraemia
 Pericardial rub
 Pruritis
 Peripheral neuropathy

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CAUSES OF CKD (RISK FACTORS) - TOP 5 CAUSES ACCOUNT FOR > 90%
1. DM
2. HT
- Due to over-activity of RAAS and sympathetic nervous system and volume overload
3. Glomerulonephritis CKD spectrum in HIV:
4. Autosomal dominant PCKD
- HT + hematuria + abd mass 1. Electrolyte + acid-base disturbance
5. Tubulo-Interstitial Nephropathy 2. Acute kidney injury
- Mostly allergic reaction to drug 3. CKD
6. Developing countries (SA) 4. Acute-on-chronic kidney disease
- Pollution + toxins (tobacco) 5. Side effects to treatment (ARV’s or
- Analgesic abuse (NSAIDs) drugs that treat Cx)
- Herbal medicine 6. Long-term metabolic s/e of ART
- HIV
7. Aging
8. Previous episode of AKI
- Acute tubular necrosis
- 2o to sepsis, hypotension, dehydration or nephrotoxicity
9. Family history of renal disease
10. Obesity

COMPLICATIONS
 Anemia
o Due to decreased production of erythropoietin (+ other factors)
 Hyperkalaemia
o Due to decreased potassium excretion
 Hyperphosphatemia /Hypocalcaemia/hyperparathyroidism
o Due to ↓ phosphate excretion and binding of phosphate to calcium
o Low s-Ca2+ and high s-PO4 stimulates PTH >> hyperparathyroidism
 Renal Osteodystrophy
o ↓renal conversion of Vit D to active Vit D >> renal osteodystrophy (painful breakdown of
bone)
 Myopathy
 Peripheral neuropathy
 Metabolic acidosis
o Decreased H+ excretion
 Edema (fluid overload due to decreased GFR )
o Due to decreased sodium excretion and Hyperaldosteronism
 Uremia
o Due to decreased excretion of urea and other toxins
o Nausea, LOA, encephalopathy (asterixis), pericarditis, ↑ bleeding (urea prevents platelet
sticking together so less clots), uremic frost (powdery skin)
 Hypertension
o Low GFR so ↑ renin release >> HPT (vicious cycle)
 Drug Toxicity
 Risk of AKI
 CVS disease (HT, stroke, MI, sudden death)
 Progress to end stage renal failure

MANAGEMENT OF CKD
1. Diagnose underlying renal disease
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2. Look for reversible factors
a. HT
b. UTI
c. Obstructions
d. Drugs (nephrotoxic)
3. Prevent further renal damage (retard progression)
o Control
 HT (ACE-i, ARBs – aim for <130/80 gradually)
 ACE-i and ARB can cause slight ↑ creat and hyper K+ with stage 3b/4/5
 DM (target HbA1c = 6.5%)
 Metformin C/I in stage 4 and 5
 2nd-gen sulphonylurea may be used if patients have no hypoglycemic episodes
 Thiazolinediones may be used in patients without heart failure or IHD
 Insulin: careful of hypoglycemic episodes (↓ renal clearance of insulin)
o Treat complications
o Diet (low protein diet, salt and fluid restriction)
o Control CVD risk factors (statin, smoking cessation, exercise, avoid NSAIDS)
4. Evaluate for renal replacement therapy
a. Dialysis
i. C/I:
- Severe CMO or refractory heart failure
- Advanced liver cirrhosis
- Terminal malignancy
- End-stage COPD
- Severe dementia
- Debilitating CVA
b. Renal transplant

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HISTORY
 History of kidney disease
 Periorbital or peripheral oedema
 Macroscopic hematuria d/t viral infection (IgA nephropathy)
 Recurrent UTI (VUR or anatomical abn)
 Past history of acute renal failure
 Sx of prostatism
 Co-morbidities: HT, DM, gout, renal stones, Infl disease (RA)
 Chronic painful conditions (excess analgesic intake)
 Drug Hx: NSAIDs, Lithium (bipolar),
 Fam Hx: kidney failure, nephrotic syndrome (>> PCKD, focal glomerulosclerosis, IgA nephropathy)

PHYSICAL EXAM:
 General: periorbital/peripheral oedema, pallor, gouty tophi, arthritis, signs of collagen vascular
disease, macroglossia (amyloidosis)
 CVS: hypertension, ESM (anaemia), pericardial friction rub (uraemia)
 Resp: pulm oedema, pleural effusion (nephrotic syndrome)
 Abd: palpable kidney (PCKD), hepatomegaly (amyloidosis), bruit (renal aa stenosis)
 Fundoscopy: HT or DM retinopathy
 Prostate gland: hypertrophy
 CNS: confusion, subtle intellectual dysfunction, muscle weakness, asterixis, peripheral neuropathy

SPECIAL INVESTIGATIONS:
 Urine:
o Dipstick (proteinuria, hematuria, leucocyte, nitrates)
o Microscopy
 Microscopic hematuria + red cell casts suggest glomerulonephritis
o Quantitation of protein excretion
 random sample’s prot:creat ratio
 Bloods:
o ANA profile, s-complement, CRP, Hep studies, uric acid, HIV, FBC (infection + anaemia),
CMP, iron studies, ALP, PTH (renal osteodystrophy)
 Severity of CKD (metabolic/haem abn):
o U+E, s-creat, eGFR (Cockcroft-gault, MDRD formula, 24h urinary creat clearance)
 Imaging:
o Renal U/S
o CT scan
 Kidney biopsy:
o Indications:
 Kidneys are normal in size, where Dx cannot be made otherwise
 Def Dx, where histology is essential for Mx (lupus nephritis, vasculitis)
 Established Dx (DM nephropathy) with unexplained ↓ in kidney fx
o C/I:
 Ilateral small kidneys
 Uncontrolled HT
 UTI or perinephric infection
 PCKD
 Bleeding diathesis
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Urine findings:
 Proteinuria (3+ most likely glomerular origin)
o Pyelonephritis, glomerulonephritis, nephrotic syndrome, diabetes, pre-eclampsia, CCF,
malignant HT, HIV nephropathy
 Hematuria (if positive, confirm with microscopy – haematuria/haemoglobinuria/myoglobinuria)
o Hematuria + proteinuria: renal or post-renal
o Urethral (stricture, trauma), bladder (infection, tumour, trauma, stone), ureter (stone),
kidney (glomerulonephritis, interstitial nephritis, tumour, trauma)
 Lucocyte + nitrates:
o UTI
 pH + specific gravity (acidosis, dehydration)
Renal function test:
 most NB = serum creatinine! (NOT serum urea)
 don’t read alone, do a eGFR (24h urine collection)