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Pulsenotes - Chronic Kidney Disease Notes PDF
Pulsenotes - Chronic Kidney Disease Notes PDF
Overview
Chronic kidney disease (CKD) can be defined by the presence of kidney damage or
reduced kidney function for three or more months.
Reduced kidney function is suggested by a reduction in the glomerular filtration rate (GFR).
Kidney damage can be characterised by the presence of one of more of the following pathological
markers.
CKD is a common condition with a progressive nature. As CKD progresses towards end-stage renal
disease (ESRD) it is associated with more symptoms, increasing complications and need for renal
replacement therapy (RRT).
The inability of the kidneys to carry out their normal function can lead to problems with volume
regulation, acid-base balance, calcium and phosphate handling and electrolyte abnormalities.
Classification
The change towards using ACR in the classification of CKD reflects the increased risk of acute on
chronic injury, end stage disease and all-cause mortality in patients with a high ACR.
CKD is increasingly common with advancing age and stages 3-5 affect up to 8.5% of the adult
population. The higher the stage of CKD, the more frequent monitoring patients require. This
helps to identify and manage complications and plan for RRT.
There are numerous causes of CKD, but the majority of cases are secondary to diabetes
mellitus, hypertension and glomerulopathies.
Hypertensive nephropathy
Diabetic nephropathy
Glomerulopathties
Inherited kidney disorders (e.g. PCKD)
Ischaemic nephropathy (e.g. vascular disease)
Obstructive uropathy
Tubulointerstitial diseases
Medications
Approximately 1 million nephrons are present in each kidney from birth. These nephrons
contribute to the kidneys ability to maintain adequate glomerular filtration and allows the kidney
to perform its normal functions (e.g. volume regulation, acid-base balance).
As we age there is a progressive loss in renal mass and a number of structural changes occur (e.g.
glomerulosclerosis) leading to a decline in renal function. Following a peak in the third decade of
life, there is an estimated annual decline of 1 mL/min/year in eGFR.
Regardless of the underlying cause, renal disease leads to progressive loss of nephrons and a
subsequent reduction in the GFR. As the disease progresses, structural abnormalities may occur
leading to kidney damage (e.g. albuminuria), and eventually, the kidneys start to lose their ability
to carry out normal functions.
Clinical features
Patients are generally asymptomatic with CKD, but start to develop non-specific symptoms
at more advanced stages (e.g. eGFR < 45ml/min).
It is always important to look for evidence of an underlying cause of CKD (e.g. large bilateral
abdominal masses could be suggestive of PCKD).
Symptoms
Signs
Pallor (e.g. anaemia)
Hypertension
Fluid overload (e.g. raised JVP, peripheral & pulmonary oedema)
Skin pigmentation
Excoriation marks
Peripheral neuropathy
Diagnosis
There are a number of ways to calculate the eGFR from serum creatinine, all should be used with
caution. Serum creatinine levels have a high individual variation changing with disease states,
muscle mass, pregnancy and dietary intake.
Many laboratories will use the Modification of Diet in Renal Disease (MDRD) equation; however,
NICE recommend the use the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI)
equation for calculating the eGFR.
Diabetes
Hypertension
Acute kidney injury
Obesity with metabolic syndrome
Cardiovascular disease
Structural renal tract disease
Proteinuria or persistent haematuria
Family history
Depending on the results of the eGFR and ACR, patients can be classified into a particular stage of
CKD. In patients with stable CKD (e.g. eGFR < 60ml/min without acute deterioration or ACR
between 3 and 70 mg/mmol), it is important to repeat these tests within 3 months. Those with
pronounced albuminuria (> 70mg/mmol) or significantly reduced eGFR (G4 or G5) require referral
to a nephrologist.
Those with evidence of persistent haematuria in the absence of infection should be investigated
for malignancy. There are a number of other referral criteria that are beyond the scope of these
notes.
Investigations
Urine
Urine dipstick
Urine microscopy
ACR (spot test)
ACR (24-hour collection)
Electrophoresis (e.g. myeloma)
Bloods
FBC
U&Es (inc. eGFR)
Bone profile
PTH
Bicarbonate
LFTs
Lipid profile
Autoimmune screen (e.g. ANCA, ANA)
Imaging
Renal ultrasound
Magnetic resonance angiography
Echocardiogram
ECG (high risk of CVS disease)
A renal ultrasound scan should be offered to patients with visible or persistent non-visible
haematuria, evidence of obstructive uropathy, family history of PCKD, reduced eGFR (< 30ml/min)
or accelerated progression of CKD.
Management
The principles of CKD management are to treat the underlying cause, prevent or slow
progression (e.g. renoprotective therapy), treat associated complications and plan for
RRT.
Renoprotective therapy
Renoprotective therapy is centered around blood pressure control and reducing proteinuria.
Specific blood pressure targets depend on whether CKD is secondary to diabetes and the
presence of proteinuria.
A standard BP target is < 130/80 mmHg if the patient is diabetic or has albuminuria. Therapy to
control BP utilises ACE inhibitors and angiotensin receptor antagonists (both renin-angiotensin
system antagonists). These drugs are both antihypertensive and antiproteinuric.
Outside of these parameters, hypertension should be treated in accordance with the usual NICE
hypertension guidance (typical target BP < 140/90 mmHg).
Statin therapy
Smoking cessation
Protein restriction
Antiplatelets for secondary prevention of CVS disease.
Treating complications
It is still important to assess patients for other potential causes of anaemia (e.g. iron-deficiency,
folate deficiency), which can subsequently be corrected. The main management for anaemia in
CKD is the use of erythropoietin-stimulating agents (ESA) such as epoetin alfa.
Hyperkalaemia
The ability of the kidneys to maintain adequate acid-base homeostasis and electrolyte
balance diminishes with worsening renal function.
Acute rises in potassium should be managed as a medical emergency. This involves stabilisation of
the myocardium (with calcium gluconate) and driving potassium into the intracellular
compartment (with insulin/dextrose).
Chronic elevations in serum potassium can be managed with low potassium diets, potassium-
binding resins and correction of acidosis.
In CKD, disorders of mineral and bone metabolism reflect a complex spectrum of pathology
that results from abnormal calcium and phosphate handling.
In disease, reduced kidney function (usually associated with a GFR < 30ml/min) leads to
hypocalcaemia, hyperphosphataemia and hyperparathyroidism (secondary
hyperparathyroidism). These biochemical abnormalities may then lead to boney pathology (e.g.
adynamic bone disease, osteomalacia, osteoporosis and osteitis fibrosa cystica). The term ‘renal
osteodystrophy’ is used exclusively for this type of bone pathology seen in CKD.
The management of mineral and bone disorders requires management of the underlying
biochemical abnormalities.
Fluid overload
In the presence of significantly reduced GFR, the kidneys are unable to adequately
controlled fluid volume.
This leads to hypervolaemia and patients may have evidence of peripheral oedema, ascites,
raised JVP, gallop rhythm and bilateral pleural effusions.
Fluid overload can be managed with a combination of fluid restriction, reduced sodium intake and
the use of oral diuretics (e.g. furosemide).
Acidosis
Patients with CKD have an increased tendency to retain hydrogen ions because of
abnormalities in their acid-base homeostasis.
Haemodialysis, peritoneal dialysis and renal transplant are all forms of RRT that are
indicated for ESRD.
In-depth analysis of the types of RRT, their indications, contraindications and efficacy are beyond
the scope of these notes. However, we will briefly cover some of the key aspects of each type.
Haemodialysis
Haemodialysis involves the removal of waste products and other substances by passing
blood through a dialysis machine.
Blood comes into contact with a semi-permeable membrane, which contains the dialysate on
the other side. Substances may then diffuse between the two fluids (blood and dialysate).
Peritoneal dialysis
Peritoneal dialysis is achieved by using the peritoneal cavity as the primary site of
ultrafiltration.
A catheter (e.g. Tenckhoff catheter) is inserted into the abdominal cavity, which allows the infusion
of the dialysate. The dialysate then dwells within the abdomen using the peritoneum as a semi-
permeable membrane for the transfer of waste products. The dialysate can then be removed after
a certain amount of time and the procedure repeated.
Renal transplant
Transplantation may be from living donors or non-living donors as long as there is MHC
compatibility, which may mediate graft rejection. Non-living donors include donors after cardiac
death (DCD) and donors after brain death (DBD).
Renal transplantation requires the use of long-term immunosuppressive therapy to stop the
recipient's immune system from ‘attacking’ the donor tissue.
Despite the overt success of transplantation, it can be associated with a number of complications
including graft rejection, complications from immunosuppressive agents (e.g. malignancy,
infection) and disease recurrence.
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