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Flashcards in Chronic Renal Failure Deck (32):

What is chronic renal failure?

Decreased GFR (<60mL/min/1.73m2) for > 3 months.

Mostly irreversible


What is the classification of chronic renal failure? Describe each stage.

What stage would you normally present with symptoms?

Each stage is determined by the GFR (mL/min)

Stage 1: >90
Stage 2: 60-89
Stage 3a: 45-69
Stage 3b: 30-44
Stage 4: 15-29
Stage 5: <15

Symptoms normally present at stage 4 (<30mL/min)


How is GFR calculated? What are the problems with this.

eGFR is a way of estimating GFR using an equation. The values you need to input are serum creatinine, age, race, and sex. This is the method currently advocated in the NHS. It is accurate it kidney disease, however, the method consistently underestimates the GRF of healthy people with a GFR of over 60ml/min.

Creatinine is a product of skeletal muscle metabolism that is produced at a constant rate and is proportional to body mass.

Serum creatinine has an exponential relationship to GFR, therefore is insensitive marker to earlier real impairment, and early small changes can indicate large drops in kidney function.

eGFR is an estimate and degree or error relating to extremes of muscle mass.

The GFR – normal GFR is about 125ml/minute.


Causes of CKD

1. Diabetes (Diabetic nephropathy) Type 2 more than type 1.

2. Glomerulonephritis: commonly IgA nephropathy also systemic disorders e.g. SLE, Vasculitis. Rare: mesangiocapillary GN

3. Unknown: 20%

4. Hypertension or renovascular disease

5. Pyelonephritis and reflux nephropathy

Hereditary: polycystic kidney disease
Drugs: NSAIDs
Rare: Urianry tract obstruction (prostatic disease)



Common disease: 6-7% in England have CKD stage 3-5.

More common in older individuals who have other medical conditions e.g. diabetes and vascular disease.

Higher rates in Black people, hispanic people and Fhx or Hx of AKI.


How do CKD patients normally present?

- Often found incidentally during other investigation or monitoring of 'at risk' individuals.

- Symtoms of CKD (late)

- Crash landers: acute presentation of undiagnosed.


Symptoms of CKD

Anaemia (lack of EPO)
- Fatigue

Platelet abnormality:
- Bruising and Epitaxsis

- Pigmentation and pruritus

GI tract:
- Anorexia, Nausea, Vomiting and Diarrhoea (toxins).

- Nocturia, Polyuria, Oedema from salt and water retention.

Hypertension, Peripheral vascular disease heart failure, uraemia pericarditis

Renal Osteodystrophy (decreased phosphate excretion, low activate of vitamin D3, high parathyroid)
- Oesteomalacia, muscle weakness, bone bone, hyperparathyroid, osteosclerosis

- Confusion, coma, fits (severe uraemia)

- Amenorrhoea, erectile dysfunction, infertility.


What is uraemia? What problems can it cause?

High levels of urea in the blood. >60mmol/L causes severe ureamic symptoms involving the CNS.

Mental slowing, confusion, seizures, myoclonic twitching, encephalopathy, coma



Brown nails
Yellow skin
High BP
Pericardial friction rub
Proximal myopathy

Signs of underlying disease:
DM: peripheral neuropathy and retinopathy


Indications for monitoring/screening?

How are they screened?

- Diabetes Mellitus
- Hypertension
- Cardiovascular disease (IHD, CCF, peripheral vascular disease, cerebrovascular disease)
- Nephrotoxic drugs (NSAIDs, Lithium)
- Structural renal disease (stones or BPH)
- Recurrent UTIs
- Multisystem illness
- Fhx of End Stage Kidney failure
- Opportunistic detection of haematuria

Bloods: eGFR
Urinalysis: proteinuria/albuminuria

Allows for early intervention and slow/prevent progression to end-stage.


Questions in Hx

Ask ureamic: anorexia, vomiting, restless leg, fatigue weakness, itching, bone pain.
Oliguria, dysponea, ankle swelling
Women: amenorrhoea
Men: impotence

To find cause:
- previous UTIs
- PMH hypertension, DM, IHD, systemic disorder, renal colic

Check drug Hx
System review


Examination and Investigations

periphery: hypertension, arteriovenous fistula (thrill, bruit) signs of previous transplant- bruising from steroids,

Face: pallor (anaemia), yellow tinge (uraemia), gum hypertrophy from cyclosporine, cushingoid appearance from steroids

Neck: Current or previous tunnelled line insertion, scar form parathyroidectomy.

Cardiovascular exam

Abdomen: peritoneal dialysis catheter or sign of previous, signs of transplant, ballot able polycystic kidney +- liver.

Elsewhere: diabetic neuropathy, retinopathy, peripheral vascular disease



FBC (normochromic, normocytic anaemia)
U&Es (raised)
Glucose (raised if DM)
Calcium (low)
Phospahte (high)
Alk Phos (high in renal otseodystrophy)
PTH: high

Dipstick (haematuria and proteinuria)
MC&S (Microscopy, Culture and Sensitivity)
Albumin:Creatinine Ratio
(Urine Microalbumin 30-300mg/day)

USS: check size/anatomy, presence of obstruction or hydronephrosis/stones

eGFR: <60mL/minute/1.73.2

Consider renal biopsy for histology (if rapidly progressive)


Who manages CKD?

Mild-Moderate= GPs

Refer to nephrologist if if:
-Stage 4/5 (eGFR <30)
- Significant Proteinuria
- Haematuria and proteinuria
- Rapidly falling eGFR
- Genetic cause
- Suspected renal artery stenosis


What are the aims of CKD management?

- Early Diagnosis
- Treat underlying cause
- Slow or prevent progression
- Prevent/Treat complications
- Timely education, planning and preparation for end-stage renal disease
- Reduce mortality
- Preserve quality of life


Treat underlying cause

Identify and treat:
relieve obstruction, stop nephrotoxic drugs, deal with high calcium and cardiovascular risk (stop smoking, weight) and tight glucose control


Limit progression, what are the 4 main factors to consider

Blood pressure, renal bone disease, cardiovascular modification and diet.


Describe management of BP

Even a small change in BP can have significant impact to BP.

CKD aim: 140/90
CKD + Diabetes aim: <130/80

Drug: local guidance but even with normal BP treat with ACEi or ARB.


Renal Bone Disease

- Treat if PTH raised
- Phosphate rises in CKD increasing PTH
- Restrict dietary phosphate (milk, cheese, eggs)
- Give binders e.g. calcichew
- Vit D analogues (alfacalcidol) and calcium supplements to decrease bone disease and hyperparathyroidism.


Cardiovascular Risk

- In stage 1/2 the risk of cardiovascular death is higher than risk of ESRF.
- Give statins (if raised lipids)
- Aspirin (low dose)



Multidisciplinary team: patient should be reviewed by a dietician for advice on healthy, moderate protein diet, K restricted if hyperkalaemic, and avoid high phosphate foods.


Name 4 main symtoms of CKD that can be controlled

Anaemia, Acidosis, Oedema and restless leg/cramps



- Check haemantics and replace iron/B12/folate if necessary.
- Consider EPO injections
- Keep Hb 100-120 g/L (above this increases risk of bleeding, increases BP and MI)



consider sodium carbonate supplements (caution if high BP as sodium load can increase BP)



- High dose loop diuretics (furosemide 250mg-2g +- metolazone (thiazide) 5-10mg/24hr po each morning
- Restrict fluid and sodium intake.


Restless leg/cramps

Check ferritin
Clonazepam (0.5-2mg daily) or gabapentin
Quinine sulphate


Prepare for renal replacement therapy.

Name 3 types of dialysis.
Describe them.

Which is used in critically ill patients?

Haemodialysis: diffusion of solutes from patients blood and dialysis fluid in artificial kidney. 4 hours 3 x week in outpatients, ideally via fistula.


Peritoneal dialysis: diffusion between patients blood in peritoneal capillaries and dialysis fluid in peritoneal cavity.
- CAPD (continuous ambulatory peritoneal dialysis) 4 x 2-3 litre exchanges a day
- APD (automated PD): several exchanges whilst asleep.



What are the options for ESRD

Peritoneal dialysis
Kidney transplantation
conservative care


Renal tranplantations. Complications

Lifelong immunosuppression.

Significant proportion of patients are not suitable for transplantation due to other medical conditions.

Surgical: bleeding, thrombosis, infection, urinary leaks

Delayed graft function: 40% of grafts, usually acute tubular necrosis due to ischaemia.

Rejection: Acute or chronic

Drug toxicity: neurological, new onset diabetes, gum hypertrophy, hirsutism..



Cardiovascular disease: leading cause of death in transplant patients


Case History

Case History

Case history
A 54-year-old man with a 10-year history of DM and hypertension, with complications of diabetic retinopathy and peripheral neuropathy, presents to his primary care physician with complaints of fatigue and weight gain of 4.5 kg over the past 3 months. He denies any changes in his diet or glycaemic control, but does state that he has some intermittent nausea and anorexia. He states that he has noticed that his legs are more swollen at the end of the day but improve with elevation and rest. Physical examination reveals an obese man with a sitting BP of 158/92 mmHg. The only pertinent physical examination findings are cotton wool patches and micro-aneurysms bilaterally on fundoscopic examination and pitting, bilateral lower-extremity oedema.

Other presentations
The disease presents insidiously over months with vague complaints of fatigue, mild reduction in appetite, and, at more advanced stages, nausea and anorexia. Oedema is a common presentation - as the GFR declines, there is an inability to effectively excrete salt and water to remain in metabolic balance with dietary intake. Additionally, proteinuria with a decrease in serum albumin may contribute to the development of peripheral oedema.


Prescribing in CKD

Impaired excretion: potential drug accumulation and serious toxicity (dose reduction or avoid)
- Digoxin, ahminoglycosides, acyclovir

- Nephrotoxins: acute reduction of renal function (NSAIDs)

- Metabolic effects: hyperkalaemia (ACEi, ARB, amiloride, spironolactone, K supplements)

- Reduced efficiency in renal failure (thiazides)


Who is involved in the care of a patient with end stage kidney disease.

- GP
- Renal physician
- Specialist renal nurses
- Dietetics
- Renal Pharmacist
- Psychologist
- Social worker, physic, OT
- Biochem, Haem, Path, Micro
- Transplant Surgeons
- Surgery for dialysis access