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Flashcards in Chronic kidney disease Deck (12):

Which three of the following are symptoms/signs of CKD?

1. Fatigue
2. Hypertension
3. Anuria
4. Polyuria
5. Pruritis

1, 2, 5
Fatigue, hypertension, pruritis

Pruritis = Ithcing
Polyuria = excessive production/passage of urine
Anuria = Failure of the kidneys to produce urine


Which of the following functions are performed by the Kidney?

1. Metabolise drugs e.g. insulin
2. First hydroxylation of vitamin D
3. Excretion of nitrogenous waste
4. Production of eryhtropoietin
5. Contributes to blood pressure control

1, 3,4,5

The first hydroxylation of vitamin D is predominantly performed by the liver. The kidney performs the second hydroxylation


What are the 2 most common causes of ESRD in the UK?

1. Chronic pyelonephritis
2. Hypertension
3. Diabetes
4. Glomerulonephritis
5. Cystinosis

2, 3


Which of the following is an absolute contraindication to renal transplant?

1. HIV
2. Active malignancy
3. Concurrent or recurrent infection
4. Diabetes
5. Age >80

2 and 3


You see Mr Jones in CKD clinic. His bloods are as follows:
CCa = 2.9 [2.2-2.6]
Phosphate = 2.0 [0.8-1.5]
PTH = 150 [1.5-7.6]

His vitamin D level is normal. He takes a maximum dose of Lanthanum (a non-calcium based phosphate binder). What treatment would help his CKD-MBD?

1. 1 alphacalcidol
2. Parathyroidectomy
3. Calcium acetate (phosphate binder)
4. Calcichew
5. Cholecalciferol

Mr Jones has evidence of tertiary hyperparathyroidism. Cholecalciferol is the inactive form of vitamin D produced by the skin from sunlight. We are told that this is normal in Mr Jones’ case therefore he does not require supplementation. Calcichew can be considered a calcium supplement (when taken between meals) or as a phosphate binder (when taken with meals). Calcium supplementation or using a calcium based phosphate binder would be inappropriate because Mr Jones has a high calcium. Similarly a vitamin D analogue such as alphacalcidol would increase the calcium and phosphate.

Management options therefore include a partial or total parathyroidectomy or using a calcimimetic such as cinacalcet. Cinacalcet is a medication that mimics calcium at calcium sensing receptors. Some of these receptors are found on the parathyroid gland and thus this new expensive drug can reduce PTH. It provides an alternative to patients who are unwilling to undergo a surgical parathyroidectomy.


Define chronic kidney disease

Chronic kidney disease is described as ‘evidence of damaged renal parenchyma as demonstrated by active urinary sediment and/or structural abnormality (this must be present for stages 1 and 2 CKD) and/or evidence of decreased kidney function as demonstrated by a reduced glomerular filtration rate (GFR) and chronicity to distinguish it from acute kidney injury (AKI).’

*Active urinary sediment = the presence of haematuria and/or proteinuria
*Structural abnormalities = Kidney stones, cysts, renal scars.

The current ­definition of CKD by KDIGO comprises:
(i) presence of kidney damage for ≥ 3 months, with kidney damage defined as pathological abnormalities or markers of damage, including abnormalities in blood or urine tests or imaging studies and/or
(ii) GFR <60 ml/min/1.73m2 for ≥ 3 months with or without kidney damage.


How is CKD staged according to GFR stage?

Normal (G1) = GFR >90 with other evidence of renal failure

Normal/mild ↓ (G2)= GFR 60-89, with other evidence of renal failure

Mild -Mod. ↓ (G3a) = GFR 45-59 with or without other evidence of renal failure

Mod - severe ↓ (G3b) = GFR 30-44, with or without other evidence of renal failure

Severe ↓ (G4) = GFR 15-29, with or without other evidence of renal failure

Kidney failure (G5) = GFR <15,
All stages


What are the signs of renal damage?

Evidence of abnormal anatomy or systemic disease


What are the causes of CKD?

Diabetes (type II >type I)
Glomerulonephritis: IgA nephropathy
Unknown (up to 20%)
Hypertension or renovascular disease
Pyelonephritis and reflux nephropathy
Polycystic kidney disease


How is CKD investigated?

Bloods – Hb, ESR, U&E, glucose, hypocalcaemia, ↑phosphate, ↑ALP, ↑PTH (if stage 3+)

Urine – dipstick, MSU, Albumin: creatinine ratio or protein: creatinine ratio

Imaging – USS kidneys,

Histology – renal biopsy


When should patients be referred to a nephrologist?

Mild-moderate CKD is usually managed in general practice. Refer to a nephrologist if the patient meets any of the following criteria:
• Stage 4/5 CKD
• Moderate proteinuria
• Proteinuria + Haematuria
• Rapidly falling eGFR (>5ml/min/1.73m3 in 1 year, or >10ml/min/1.73m3 within 5 years)
• Hypertension poorly controlled despite at least anti-hypertensive drugs
• Known/suspected rare or genetic causes of CKD
• Suspected renal artery stenosis


How is CKD managed?

1) Identify and treat reversible causes;
-Relieve obstruction, stop nephrotoxic drugs, deal with high calcim, and cardiovascular risk, improve glucose control

2) Limit progression/ complications:
- Blood pressure: target BP should be <130/80mmHg
- Renal bone disease (risk of osteodystrophy or adynamic bone disease). Check PTH and treat if raised. Phosphate is raised in CKD, which further ↑PTH and precipitates in the kidney and vasculature. Restrict diet, give binders (calci-chew) to decrease gut absorption. Vitamin D analogue (alfacalcidol) and calcium supplements decrease bone disease and hyperparathyroidism.
- Cardiovascular modification: Statin and aspirin
- Diet: healthy moderate protein diet, K+ restriction I hyperkalaemic, avoid high phosphate foods

3) Management – Symptom control
- Anaemia: Iron/B12 replacement
- Acidosis: sodium bicarbonate supplements
- Oedema: high dose loop diuretic, restricted fluid ad sodium intake
- Restless legs/cramps: check ferritin, clonazepam, gabapentin, quinine sulfate

4) Management - Renal replacement therapy