Chronic Kidney Disease Flashcards by Andrew Hay

What is the traditional definition of chronic renal failure?

Irreversible and significant loss of renal function

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How do we assess for kidney disease?

Excretory function
-Glomerular Filtration Rate (eGFR from creatinine blood test)

Filtering function
-Check for presence of blood or protein in urine

Anatomy
-Histology, radiology

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What is the problem with the relationship between serum creatinine and GFR (for measuring eGFR)?

Creatinine will not be raised above the normal range until 60% of total kidney function is lost

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What effects serum creatinine levels?

Muscle mass:

Age,
Ethnicity (African Americans)
Gender (Male)
Weight

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Give some formulae to estimate GFR from serum creatinine

Cockcroft Gault

MDRD 4 variable equations

CKD-EPI equation

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What crosses the GBM?

Water
Electrolytes
Urea
Creatinine

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What crosses the GBM but is reabsorbed in the proximal tubule?

Glucose

Low molecular weight proteins (a2-microglobulin)

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What doesnt cross the GBM?

Cells (RBC, WBC)

High molecular weight proteins (albumin, globulins)

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How much blood or protein should you be able to measure in a normal kidney?

Should be no blood or protein measurable in urine if filtering properly

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How can you test for protein or blood in urine?

Urinalysis (“dipstick”)

Blood
Protein

Protein quantification
-Protein creatinine ratio (PCR)

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What is the current chronic kidney disease definition?

Chronic kidney disease is defined by either the presence of kidney damage (abnormal blood, urine or x-ray findings) or GFR /= 3 months

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What is the prevelence of CKD?

Increases with age

About 8-12% in UK

Mostly stage 3

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Give some of the complications of chronic kidney disease

Acidosis
Anaemia
Bone disease
Cardiovascular
Death and dialysis
ELectrolytes
Fluid overload
Gout
Hypertension
Iatrogenic issues

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How much does CKD cost?

About £35,000pa for 1 patient

Around £6,500 drug costs
£20,000 transplant

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What is the aetiology of CKD?

Polycystic kidney disease

Diabetes

Glomerulonephritis
-And all the causes of that

Hypertension

Renovascular disease

etc

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What is the clinical approach to CKD?

Detection of the underlying aetiology
-Treatment for specific disease

Slowing the rate of renal decline
-Genetic therapies

Assessment of complications related to reduced GFR
-Prevention and Treatment

Preparation for Renal replacement therapy

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What are you looking for in terms of previous evidence of renal disease in a CKD history

Raised urea/ creatinine

Proteinuria/ haematuria

Hypertension

LUTS

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What systemic diseases do you need to keep an eye out for in a CKD history?

Diabetes Mellitus

Collagen vascular diseases:
-SLE, Scleroderma, Vasculitis

Malignancy:
-Myeloma, Breast, lung, lymphoma

Hypertension

Sickle cell disease

Amyloidosis

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What drugs are you keeping an eye out for in CKD history?

NSAIDs

Penicillins/ aminoglycosides

Chemotherapeutic drugs

Narcotic abuse

ACE inhibitor/ ARBs

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What uraemic symptoms may you be looking for in a CKD history?

Nausea, anorexia, vomiting

Pruritus

Weight loss

Weakness, fatigue, drowsiness

What are some of the clinical signs of depleted volume status?

Orthostatic BP

Skin turgor/ temperature

What are some of the clinical signs of fluid overload?

Raised JVP

Crepitations

Ascites

Oedema

What chemistry investigations may you want to carry out to look for CKD aetiology?

U&E (Na, K, Cl)

Creatinine

Bicarbonate

Total protein, albumin

Calcium, phosphate

Liver function tests

Creatine Kinase

Immunoglobulins, serum protein electrophoresis

What haematology investigations may you want to carry out to look for CKD aetiology?

FBC

Hb
MCV
MCH
WBC
Platelets
% hypochromic RBCs

What will be included in a coagulation screen you may want to carry out?

PT APPT +/- Fibrinogen

What imaging may you want to carry out to find the aetiology of CKD?

Ultrasound Plain radiology CT Nuclear medicine MRI

When can pathology be useful for finding the aetiology in CKD?

Unexplained renal failure and Normal sizes kidneys

How can you slow the rate of renal decline?

BP control Control Proteinuria Reverse other contributing factors - treat causes Others: - Allopurinol - Dietary proetin restriction - Fish oils - Lipid lowering - Control acidosis

What investigations can you carry out to assess complications related to reduced GFR?

Blood count and Film - ?Anaemic Calcium Phospate Albumin PTH - ?Renal bone disease Creatine Urea - ?GFR Bicarbonate - ?Acidosis Electrolytes - ?Hyperkalaemia Urine Protein excretion (Pr:Cr) - ?Degree of proteinuria

When does anaemia usually manifest in CKD?

When GFR

Describe the anaemia resulting from CKD?

Normochronic Normocytic Reduced erythropoietin production Reduced red cell survival Increased blood loss

How do you treat anaemia due to CKD?

Usually treat if

When is metabolic acidosis usually seen in CKD? When is metabolic acidosis most marked?

Nor usually seen until GFR

What are the symptoms of metabolic acidosis due to CKD?

General symptoms Worsens hyperkalaemia Exacerbates renal bone disease

How do you treat metabolic acidosis in CKD?

Treat with oral Na Bicarbonate | -Care with volume overload

How does CKD result in bone disease?

Reduced GFR leads to hyperphosphataemia Loss of renal tissue leads to lack of vitamin D -(indirect reduction in Ca absorption) Low Calcium and raised phosphate Secondary hyperparathyroidism (elevtaed PTH) May progress to tertiary hyperparathyroidism

How does CKD effect activation of vitamin D?

Vitamin D, derived from sunlight or diet, requires to be hydroxylated to be active - 1,25 (OH) 2 D The 1a hydroxylation is catalysed by 1a hydroxylase in the kidney CKD -> low 1a hydroxylase, so low activation of vitamin D

How does low vitamin D lead to low calcium?

Reduced intestinal absorption Reduced tubular reabsorption Resulting stimulation of PTH secretion (i.e. secondary hyperparathyroidism)

What does high phosphate levels cause?

Reduced 1a hydroxylase therefore low vitamin D Stimulates PTH production Associated with vascular and cardiac calcification

How do you manage renal bone disease?

Control phosphate -Diet - Phosphate binders - --CaCO3, Ca Acetate, Sevelamer, lanthanum Normalise Calcium and PTH -Active Vit D analogues (Calcitriol) - Tertiary disease - --Parathyroidectomy and Calcimetics (Cinacalcet)

Why does CKD result in Hyperkalaemia?

Normally excreted by exchange with Na+ in distal tubule Reduced delivary of Na+ to distal tubule as GFR falls Other factors include underlying disease, drgs and diet

How do you treat acute hyperkalaemia?

Stabilise cardiac membrane -Calcium Gluconate Shift K+ into cells - Salbutamol - Insulin-Dextrose Remove calcium from body: - Dialysis - Calcium resonium

How do you treat chronic hyperkalaemia?

Diet Drug modifications

When does fluid/ volume overload become problomatic in CKD?

When GFR

How does CKD lead to fluid/ volume overload?

Unable to excrete an excess Na+ load Na+ and water retention Oedema and hypertension

How do you treat fluid overload in CKD?

Na+ restriction Fluid restriction Loop diuretics

How do you tackle hypertension in CKD?

Treatment as per slowing rate of progression Most imporatnt in proteinuric renal disease ACEI may offer additional advantage Otherwise tailored therapy Aim

What drugs should by be weary of in CKD?

The main effect of kidney disease is reduced excretion of drugs and their toxins -Beware antibiotics, morphine, digoxin, metformin amongst others In those with CKD certain drugs and agents can cause acute kidney injury on top of CKD: -Contrast agents, antibiotics

What is associated with worse outcomes in CKD?

Worse kidney function (GFR) More proteinuria