Chronic Renal Failure Flashcards
What are the common symptoms of patients suffering from chronic kidney failure?
Anaemia:
Malaise, loss of appetite
Renal:
Nocturia and polyuria
Insomnia (secondary to nocturia)
Uraemia:
Nausea, vomiting and diahorrea.
Fluid overload:
Leg swelling (peripheral oedema)
SOB (pulmonary oedema)
Symptom usually only occur at stage 4 renal failure
End stage renal failure can present with oliguria, however failure of tubular reabsorption will lead to very high urine output.
What are the initial investigations you would do for a patient with CKD?
To assess:
Renal function: eGFR
FBC: check for anaemia
Urinalysis: check for presence of protein
Autoantibodies screen if goodpasture’s suspected
ECG: if any complaints/signs of pulmonary oedema
What are some complications of chronic renal failure?
Blood:
Anaemia (reduced renal erythropoietin synthesis)
Coagulopathy
Bone disease:
Renal osteodystrophy secondary to secondary hyperparathyroidism.
Kidneys normally convert Vit D into its active form. In its active form it causes Ca reabsorption from the intestine. The Kidneys also excrete phosphate and reabsorb calcium, when damaged however they cannot do this.
The net result is low serum Ca and high phosphate. The low Ca levels result in more parathyroid hormone being produced. This means that there is increased osteoclast function and more Ca is reabsorbed from the bones causing osteodystrophy.
Fluid:
Pulmonary oedema
Hypertension
Cardiac:
Left ventricular hypertrophy
Heart failure
Neurological:
Uraemic encepalopathy
Endocrine:
Glucose intolerance due to peripheral insulin resistance
K+
Arrhythmias
What is autosomal dominant polycystic kidney disease?
Inherited disorder usually presenting in adult life (40-60 half have stage CKD by 60)
Characterised by the development of multiple renal cysts. The cysts compress areas of the kidney and eventually replace much of the renal tissue.
This causes progressive renal impairment sometimes punctuated by acute episodes of loin pain and haematuria. Often associated with the development of hypertension.
Caused by PKD1 and PKD2 genes.
Describe the pathophysiology of diabetic nephropathy?
Glomerular hyperfiltration (hyperglycaemia thought to cause increased cell growth in the kidneys)
Intraglomerular hypertension
Glomerular basement membrane thickening
Expansion of mesanginal cells
Nodular scelrosis
How does diabetic nephropathy present? What is the treatment?
Proteinuria specifically hyperalbuminuria
Treat with ACE inhibitors
Note: usually preceded by retinopathy
Describe the different classifications of CKD based on eGFR?
1 >90 2 60-89 3a 45-59 3b 30-44 4 15-29 5 Less than 15
What are some of the signs you may find on examination?
Uraemia: Increased skin pigmentation, excoriation
Anaemia: Pallor
Fluids: Hypertension, postural hypotension, peripheral oedema, pleural effusions
Cardiac: left ventricular hypertrophy
Describe how pyelonephritis can cause CKD?
Pyelonephritis is infection of the renal pelvis often accompanied by infection of the renal parenchyma.
It is often an ascending infection from the urinary tract..
Following infection there can be fibrosis, reduced renal function and GFR.
What is interstitial nephritis?
It is inflammation of the tubule or interstitium.
What usually causes interstitial nephritis?
It is usually caused by a drug hypersensitivity reaction which causes damage and necrosis in the tubo-interstitium.
Chronic intersitital nephritis is usually caused by a build up of the nephrotoxic metabolites of phenacetin/paracetamol.
Other known nephrotoxic drugs are:
- 5 ASA
- Ciclosporin
- Lithium
How does hypertension cause renal damage?
Chronically high BP or very high BP causes damage and narrowing to the renal aa therefore causing hypo perfusion to the kidneys.
It can also cause damage to the capillaries supplying the nephrons causing the nephrons to die.
How does ureteric obstruction cause renal damage and CKD?
Ureteric obstruction causes distal ureteric dilation (painful).
It causes there to be increased back pressure which can cause renal tubular atrophy.
In response to the back pressure the glomerulus undergoes fibrosis.
All of these mechanisms result in a decreased GFR and therefore a degree of CKD.
Describe the type of anaemia which occurs in CKD?
In severe CKD (stage 4) patients often develop anaemia.
This is usually due to a reduced renal synthesis of erythropoietin. In this case the anaemia will be normochromic and normocytic.
Iron deficiency is also common in patients with CKD due to poor dietary intake. In this case the anaemia will be microchromic and microcytic.
How should anaemia in CKD be managed?
Should be managed in secondary care.
Should be treated when Hb is less than 110.
Treatment should be with erythropoiesis-stimulating agents and if there is a degree of iron deficiency this should be corrected.
Contraindications of erythropoiesis stimulating agents is uncontrolled hypertension as it can increase BP as a side effect.