JC79 (Medicine) - Chronic kidney diseases Flashcards by Max Kam

Clinical definition of CKD

GFR < 60 mL/min/1.73m2 for ≥ 3 months (Normal range = 90 – 120 mL/min/1.73m2)
Evidence of kidney damage such as albuminuria for ≥ 3 months
Abnormal findings on renal imaging present for ≥ 3 months

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Define range of GFR for 5 stages of renal failure

Stage 1 - Normal >90 
Stage 2 - Mild decrease 60-89
Stage 3 - Moderate decrease 45-59
Stage 3b - moderate to Severe decrease 30-44
Stage 4 - Severe decrease 15-29 
Stage 5 - End-stage - <15

** must be sustained for >90 days **

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How does albuminuria affect prognosis of CKD

Higher persistent albuminuria = worse prognosis and higher risk of progression in CKD

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Basic functions of nephron unit

Remove nitrogenous waste product
Conserve Sodium and water
Maintain electrolyte balance
Maintain acid-base balance

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Albuminuria

- Cut-offs for normal vs diabetic pt.

Urine Albumin-creatinine ratio > 30mg/mmol = significant albuminuria in normal pt.

Urine ACR >3mg/mmol = microalbuminuria in diabetic pt., need ACEI or ARB

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3 formulas for estimated GFR

Cockcroft and Gault Creatinine Clearance: age, serum creatinine, weight

Modification of Diet in Renal Disease Study (MDRD)

CKD- EPI or CKD- EPIcys

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Most common causes of CKD

DM nephropathy (45%) **
Hypertension/ Renal artery stenosis (RAS) (27%)
Chronic Glomerulonephritis (10%)
Chronic pyelonephritis
Interstitial disease (5%)
Polycystic kidney disease (2%)
Drug induced (TCM)
Myeloma (CARB), Vasculitis, SLE
Obstruction, nephrolithiasis
Hereditary diseases (e.g. Alport’s)

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Define pre-renal causes of CKD

Hypovolemia
• Hemorrhage
• Vomiting/ Diarrhea
• Diuretics

Hypervolemia but low effective circulating volume
• Heart failure with reduced ejection fraction (HFrEF)
(Cardiorenal syndrome)
• Decompensated liver disease with portal hypertension (Hepatorenal syndrome)

Low Afferent arteriole vasodilatation
• NSAIDs - Inhibits COX enzymes and thus decreased synthesis of prostaglandins (PG)
• ACEI/ ARB
• Cyclosporine

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Define renal causes of CKD

Renal vascular disease:
 Hypertensive nephrosclerosis
 Ischemic nephropathy - Renal artery stenosis

Glomerular disease:
 Proliferative glomerulonephritis (Nephritic pattern)
 Non-proliferative glomerulonephritis (Nephrotic pattern)

Tubular-interstitial diseases: 
 Polycystic kidney disease (PKD)
 Reflux nephropathy
 Nephrocalcinosis - Result of hypercalcemia or hypercalciuria
 Sarcoidosis

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List proliferative and non-proliferative primary glomerulonephritis

 Proliferative glomerulonephritis (Nephritic pattern)
• Post-streptococcal glomerulonephritis (PSGN)
• IgA nephropathy
• Membranoproliferative glomerulonephritis

 Non-proliferative glomerulonephritis (Nephrotic pattern)
• Minimal change disease (children)
• Focal segmental glomerulosclerosis
• Membranous nephropathy (adult)

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Post-renal causes of CKD

Obstructive uropathy
 Prostatic disease
• Benign prostatic hyperplasia
• Prostatic cancer

 Metastatic disease

+ other obstructive pathologies…etc

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Common renal symptoms between AKI and CKD

How to distinguish from AKI

Edema (hypoalbuminemia and RAAS activation)

Hypertension (fluid retention and low plasma volume triggers compensatory RAAS activation for salt and water retention

Oligouria

"”CKD has complications in CVD, Neuro, Haemat, endocrine…etc””
Anuria is never observed in CKD alone, always indicate AKI

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Determinants of CKD progression

Typical GFR deterioration rate

Underlying cause
Baseline serum creatinine and severity of proteinuria
Hypertension severity
Renal fibrosis and aging

Rate: From 1ml/min to 7ml/min over 1 year

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Mild CKD does not require management as it does not correlate with mortality.

True or False?

False

Mild CKD and albuminuria increases risk of cardiovascular death

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Cardiovascular complications of CKD

Uremic pericarditis*/ Hypertension/ Hyperlipidemia/ Cardiomyopathy/ Accelerated atherosclerosis/ Volume overload/ Congestive heart failure

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Neurological complications of CKD

Uremic encephalopathy* (Mental status change/ Coma/ Decreased in memory and attention)/ Neuropathy/ Seizure/ Impaired sleep

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Hematological and endocrine complications of CKD

Hematological
Uremic bleeding* (Platelet dysfunction and EPO deficiency)/ Anemia

Endocrinological
Hyperkalemia/ Hyperphosphatemia/ Hypocalcemia/ Metabolic acidosis/ Secondary hyperparathyroidism/ Renal osteodystrophy

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Dermatological complications of CKD

Dermatological
Pruritus*/ Calciphylaxis/ Nephrogenic systemic fibrosis (NSF)/
Uremic frost (white crystals in and on the skin)

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Constitutional symptoms of CKD

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Fatigue/ Anorexia/ Nausea and vomiting*/ Metallic taste/ Fetor uremicus
Nocturia/ thirst

Outline history taking for CKD

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Medical history
• Hypertension (Hypertensive nephrosclerosis)
• DM (DM nephropathy)
• Previous AKI
• Cardiovascular/ Cerebrovascular/ Peripheral vascular disease for renovascular disease

Drug history
• NSAIDs/ Cisplatin/ Cyclosporine

Family history
• Polycystic kidney disease
• IgA nephropathy
• Hereditary nephropathy
• C3 glomerulonephritis

Drug-induced kidney failure

Define time cut-off for acute, subacute and chronic
Pathogenesis pathways

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Acute = <7 days 
Subacute = 7-90 days 
Chronic = >90 days

Pathogenesis pathways:

Hypersensitivity
Vasoconstriction and hypoxic damage
Glomerular disease
Tubular toxicity
Nephrolithiasis and Crystalluria

List example of drug-induced AKI

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Protease inhibitor 
Cisplatin 
Aminoglycosides 
Acyclovir 
Calcineurin inhibitor ...etc

Major clinical features of CKD

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Constitutional: Fatigue, Nocturia and thirst, fluid retention and edema, General pruritis

CVS: Hypertension, LVH, Congestive HF

Anaemia (NcNc)

CKD- Mineral bone disorder: includes abnormal PTH, bone biochemistry, vascular calcification

Diagnostic investigations for CKD

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Ultrasound Kidney: Small/dysplastic/shrunken kidney
CT angiogram for vascular causes of CKD
Renal biopsy with histological diagnosis

Treatment targets for CKD (what needs to be treated/controlled in CKD)

- Delay renal failure - Treat cardiac, neurological, vascular risk, prevent CKD complications - Control albuminuria by ACEi or ARB - Control DM, HTN - Correct electrolyte and acid-base disturbance - Correct Lipid profile

Typical CBC, Lipid, Electrolyte, ABG, PTH, RFT profile in CKD

CBC - NcNc anaemia Lipid - Hypertriglyceridemia (reactive to low albumin) HypoNatremia HyperKalemia (K+ shift due to metabolic acidosis) HypoCalcemia (low Calcitriol production, sec. to hyperphosphatemia) HyperPhosphatemia (low renal excretion) ABG: Metabolic acidosis + ↑ Anion gap PTH: ↑ PTH level due to secondary hyperparathyroidism RFT: ↑ Urea/ BUN and creatinine level; ↓ GFR

List all serological and urine tests for CKD

``` CBC with diff. Lipid profile Electrolyte with Ca and PO4 ABG Serum PTH RFT: Urea/ BUN and creatinine, GFR Urinalysis: quantitative protein test ``` Autoimmune markers: ANA/ anti-dsDNA/ C3/4/ ANCA/anti-GBM Serum free light chain assays Serum/ Urine protein electrophoresis with immunofixation LFT: hepatorenal syndrome, high ALP HBV and HCV (urgent HD)

Imaging and sampling Ix for CKD

Renal biopsy for histological Dx with light microscopy, EM and immunofluorescence Imaging: X-ray or CT KUB USG kidney ***MRI avoided- administration of gadolinium is associated with potentially severe syndrome of nephrogenic systemic fibrosis (NSF) **

Dietary modifications for CKD

Calories: 30 – 35 kcal/kg/day Vitamins: Ascorbic acid, Folate, Calcitriol Low Sodium: reduce to <2g (<90mmol) for Hypertensive Low Potassium: < 1 mmol/kg/day Low PO4: < 800 mg/day Low protein: - for CKD stage 3-5: reduce uremic toxins and clinical symptoms - Diabetic Nephropathy: 0.8g/kg

Lipid control for CKD - Drug option - Indication - Risk of no control

Indications: - >50 years old - CKD 3-5 Drugs: Statin +/- Ezetimibe Risk: 10% CVD risk in 10 years

Diabetic control in CKD - Treatment/ drug options - eGFR cut-offs for different treatments

1. Lifestyle control: physical activity, nutrition, weight loss 2. First-line: - Metformin** - SGLT2 inhibitor ** 3. Additional drugs: - GLP-1 receptor agonist *preferred* - DPP-4 inhibitor - Insulin - Sulphonylurea - TZD - Alpha- glucosidase inhibitor Cut-off: - Discontinue/ do not initiate Metformin or SGLT2 inhibitor if eGFR <30 - Stop Metformin or SGLT2 inhibitor if on dialysis

Electrolyte and acid-base correction therapy for CKD

Hyperkalemia • Calcium gluconate/ Dextrose-insulin infusion/ Sodium bicarbonate/ Resonium C • Restriction of dietary K+ intake, discontinuation of ACEI/ ARB Hypocalcemia • Calcium gluconate or calcium carbonate if symptomatic • Restriction of dietary PO43- intake Hyperphosphatemia • PO43- binding agents Metabolic acidosis • Sodium bicarbonate or sodium citrate • Initiation of dialysis

Anaemia treatment in CKD - Target Hb - Tx options

Symptomatic anemia • Target Hb = 10-11 g/dL Treatment: • Blood transfusion preferably during dialysis using packed cells • Erythropoiesis stimulating agents/ ESA (EPO therapy) in refractory anemia • Iron supplementation (transferrin saturation >20%)

CKD- Bone mineral disease | - Tx options

Active vitamin D analogues - Alfacalcidol Calcimimetics Parathyroidectomy Phosphate Binders and dietary phosphate restriction

Outline Vitamin D metabolism in skin, liver and kidney

CKD-MBD - Features - Pathogenesis

Definition: • Abnormalities of Ca2+, PO43-, PTH and vitamin D metabolism • Abnormalities in bone turnover, mineralization, volume linear growth or strength Pathogenesis: - Hyperphosphatemia + Vitamin D deficiency (1a hydroxylase) + Secondary hyperparathyroidism

Phosphate binding agents for CKD - Types - Indication of use for each type

Main types: Calcium binding and Non-calcium binding Indications: LOW Ca2+ = Calcium acetate or calcium carbonate HIGH Ca2+ = Sevelamer (Renagel)/ Lanthanum (Fosrenol) - NON-calcium-NON-aluminium containing binders

MoA of non-calcium containing phosphate binding agents

 Sevelamer is a non-absorbable cationic polymer that bind PO43- in intestinal lumen through ion exchange limiting absorption  Lanthanum is a rare-earth element that lowering PO43- level

Clinical manifestations of CKD-BMD

``` Bone: Ostetis fibrosa cystica Adynamic bone disease Osteoporosis Mixed uremic osteodystrophy Gout and pseudogout ``` Vascular calcification: Coronary artery calcification (death) Calciphylaxis (small vessel calcification in fat and skin)

Pathogenesis of Osteitis fibrosa cystica, Adynamic bone disease, Osteomalacia and Mixed uremic osteodystrophy in CKD-BMD

Osteitis fibrosa cystica o (↑ PTH) High bone turnover due to secondary hyperparathyroidism Adynamic bone disease o (↔/↓ PTH) Low bone turnover, reduced bone volume and mineralization o Due to excessive suppression of parathyroid gland by vitamin D use, calcium-based phosphate binder or calcium-dialysis solution Osteomalacia o (↔/↓ PTH) Low bone turnover and abnormal mineralization o Due to use of aluminum-based phosphate binder Mixed uremic osteodystrophy o High or low bone turnover and abnormal mineralization

List bone abnormalities caused by CKD-BMD

Subperiosteal resorption Fracture Bone pain Metastatic calcifications

Management options of CKD-BMD

- Low dietary PO4 intake - Calcium-containing PO4 binding agents such as calcium acetate - Calcitriol or vitamin D analogues - Calcimimetics (stimulate parathyroid CaSR to decrease PTH secretion) - e.g. Cinacalcet - Total parathyroidectomy with autotransplantation

Calciphylaxis Definition Ix Tx

Calcification of media of small-to-medium-sized vessels of dermis and subcutaneous fat, causes skin ischemia and necrosis with painful lesions Ix: Skin biopsy Tx: Sodium thiosulfate* (IV/ Intralesional) Cinacalcet or parathyroidectomy for hyperparathyroidism NON-calcium-containing phosphate binder for hyperphosphatemia

Which treatment for CKD-BMD is appropriate if there is Calciphylaxis Which treatment is not indicated

Aim for lower Ca: Canacalcet** (Calcimimetics) Lower Ca, PTH, PO4 Not indicated: Calcium-containing phosphate binding agents Vitamin D analogues/ Calcitriol

What causes of abnormal skin complexion in CKD

 Coexistence of anemia and retention of β-melanocyte-stimulating hormone  Pigment deposition (urochromogens)

Indications for emergency dialysis in CKD

* Respi: Acute pulmonary edema * CVS: Uremic pericarditis or cardiac tamponade * CNS: Uremic encephalopathy * Endo: Severe metabolic acidosis * Endo: Hyperkalemia

JC79 (Medicine) - Chronic kidney diseases Flashcards

(46 cards)