CKD implies longstanding, and usually progressive, impairment in renal func-tion. It is defined on the basis of persistent (>3 months) evidence of kidney damage (proteinuria, haematuria, or anatomical abnormality) and/or impaired glomerular filtration rate (Table 9.14). Patients at risk of CKD, e.g. with dia-betes mellitus or hypertension, should be regularly screened to look for evidence of disease.
|Emergency Box 9.1|
|Principles of management of a patient with acute
To prevent death from hyperkalaemia (p. 340) or pulmonary oedema (p. 443).
Establish the aetiology and treat the underlying cause
• History, including family history, systemic disease, use of nephrotoxic drugs
• Examination includes assessment of haemodynamic status, pelvic and rectal examination
• Investigations (p. 387). May include bladder catheterization or flush of existing catheter to exclude obstruction
Prevention of further renal damage
Early detection of infection and prompt treatment with antibiotics. Avoid hypovolaemia, nephrotoxic drugs, NSAIDs and ACE inhibitors.
Management of established renal failure
• Seek advice from a nephrologist
• Once fluid balance has been corrected, the daily fluid intake should equal fluid lost on the previous day plus insensible losses (approximately 500 mL)
• Diet – enteral nutrition is preferred over parenteral. Sodium and potassium is restricted
• Nursing care, e.g. prevention of pressure sores
• Adjust doses of drugs that are excreted by the kidney, and monitor serum drug levels where appropriate (refer to national formulary for guidance)
• Monitor daily: serum biochemistry, fluid input and output and bodyweight to assess fluid balance changes
• Frequent review regarding the need for dialysis
Careful fluid and electrolyte balance during recovery phase
Large volumes of dilute urine may be passed until the kidney recovers its concentrating ability.
NSAIDs, non-steroidal anti-inflammatory drugs; ACE, angiotensin-converting enzyme.
Causes of CKD vary depending on geographical area, racial group and age. Diabetes mellitus, hypertension and atherosclerotic renal vascular disease are the most common causes in European countries (Table 9.15). In parts of the Middle East, schistosomiasis is a common cause due to a ureterovesical
|Table 9.13 Indications for dialysis and/or haemofiltration in acute kidney injury (AKI)|
|Progressive uraemia with encephalopathy or pericarditis
Severe biochemical derangement especially if there is a rising trend in an
oliguric patient and in hypercatabolic patients
Hyperkalaemia not controlled by conservative measures
Severe metabolic acidosis: pH < 7.1
For removal of drugs, causing the AKI, e.g. gentamicin, lithium, severe aspirin
Table 9.14 Classification of chronic kidney disease
Formulae based on SCr
eGFR < 60 mL/min/1.73 m2
Early morning urine sample
ACR ≥ 30 mg/mmol or PCR ≥ 50 mg/mmol
>1+ and urological causes excluded
(e)GFR, (estimated) glomerular filtration rate; SCr, serum creatinine; ACR,
stricture causing urinary tract obstruction. Regardless of the underlying cause, fibrosis of the remaining tubules, glomeruli and small blood vessels results in progressive renal scarring and loss of renal function in some individuals.
Clinical features and investigations
The early stages of renal failure are often completely asymptomatic. With a declining GRF and an associated rise in serum urea and creatinine concentra-tions there is an accumulation of symptoms and signs described below. The actual metabolites that are involved in the genesis of many of these clinical features is not known (Figure 9.6). Investigations are similar to those in AKI (p. 387).
Anaemia is primarily due to reduced erythropoietin production by the diseased kidney. Shortened red cell survival, increased blood loss (from the gut, during haemodialysis and as a result of repeated sampling) and dietary deficiency of haematinics (iron and folate) also contribute.
Bone disease The term ‘renal osteodystrophy' embraces the various forms of bone disease that develop in CKD, i.e. osteomalacia, osteoporosis
|Table 9.15 Causes of chronic kidney disease|
|Congenital and inherited disease
Polycystic kidney disease (adult and infantile forms)
Congenital obstructive uropathy
Other rare causes
Secondary glomerular disease, e.g. diabetes mellitus, amyloidosis, SLE
Hypertensive nephrosclerosis (common in black Africans)
Small and medium-sized vessel vasculitis
See page 374
Urinary tract obstruction
Any causes of chronic obstruction (p. 381).
SLE, systemic lupus erythematosus.
secondary and tertiary hyperparathyroidism and osteosclerosis. Renal phos-phate retention and impaired production of 1,25-dihydroxyvitamin D (the active hormonal form of vitamin D) lead to a fall in serum calcium concentra-tion and hence to a compensatory increase in parathyroid hormone (PTH) secretion. A sustained excess of PTH results in skeletal decalcification with the classic radiological features described in Fig. 9.7. Osteosclerosis (harden-ing of bone) may be a result of hyperparathyroidism.
Neurological complications occur in almost all patients with severe CKD and are improved by dialysis. Polyneuropathy manifests as peripheral par-aesthesiae and weakness. Autonomic dysfunction presents as postural hypo-tension and disturbed gastrointestinal motility. In advanced uraemia (serum urea >50-60 mmol/L) there is depressed cerebral function, myoclonic twitching and fits. Median nerve compression in the carpal tunnel is common and is usually caused by β2-microglobulin-related amyloidosis (a complica-tion of dialysis).
Cardiovascular disease The highest mortality in CKD is from cardio-vascular disease particularly myocardial infarction, cardiac failure, sudden cardiac death and stroke. This occurs due to an increased frequency of hypertension, dyslipidaemia and vascular calcification. Renal disease also
Fig. 9.6 Symptoms and signs of chronic kidney disease. Oedema may be due to a combination of primary renal salt and water retention and heart failure. GI, gastrointestinal.
results in a form of cardiomyopathy with both systolic and diastolic dysfunc-tion. Pericarditis and pericardial effusion occurs in severe uraemia.
Other complications include an increased risk of peptic ulceration, acute pancreatitis, hyperuricaemia, erectile dysfunction and an increased incidence of malignancy.
Differentiating AKI from CKD
Distinction between AKI and CKD depends on the history, duration of symp-toms and previous urinalysis or measurement of serum creatinine. A
Fig. 9.7 Renal osteodystrophy. Pathogenesis and radiological features of renal bone disease. ALP, alkaline phosphatase.
normochromic anaemia, small kidneys on ultrasonography and the presence of renal osteodystrophy favour a chronic process.
The aims of treatment are:
■ Specific therapy directed at the underlying cause of renal disease, e.g. immunosuppressive agents for vasculitis and tight metabolic control in diabetes
■ Slow deterioration of kidney function (renoprotection)
■ Reduce cardiovascular risk
■ Treat the complications, e.g. anaemia
■ Appropriate dose adjustment of prescribed drugs based on guidance in a national formulary.
The goal of treatment should be to maintain the blood pressure at less than 120/80 mmHg and to maintain a urinary protein concentration of less than 0.3 g/24 hours. Good blood pressure control may slow the decline in renal function.
Patients with CKD and proteinuria >1 g/24 hours should receive:
■ ACE inhibitor, increasing to maximum dose
■ Angiotensin receptor antagonist if goals are not achieved; in diabetes mellitus start with angiotensin receptor antagonist
■ Diuretic to prevent hyperkalaemia and help to control blood pressure
■ Calcium-channel blocker (verapamil or diltiazem) if goals not achieved.
Reduce cardiovascular risk
■ Optimal control of BP and reduction of proteinuria (as above).
■ Statins to lower cholesterol to <4.5 mmol/L.
■ Cessation of smoking.
■ Optimize diabetic control, HbA1c <7%.
■ Normal protein diet (0.8-1 g/kg bodyweight/day)
Correction of complications
Hyperkalaemia often responds to dietary restriction of potassium intake. Drugs which cause potassium retention should be stopped. Occasionally it is necessary to prescribe ion-exchange resins to remove potassium in the gastrointestinal tract. Emergency treatment of severe hyperkalaemia is described on page 340.
Calcium andphosphate Hyperphosphataemia is treated by dietary phos-phate restriction and administration of oral phosphate-binding agents such as calcium carbonate (contraindicated with hypercalcaemia or hypercalci-uria), sevelamer or lanthanum carbonate. The serum calcium should be maintained in the normal range through the use of synthetic vitamin D ana-logues such as 1α-cholecalciferol or the vitamin D metabolite 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3).
Anaemia Iron deficiency is common in patients with CKD and should be treated. Recombinant human erythropoietin is an effective but expensive treatment for the anaemia of CKD. It is administered subcutaneously or intravenously three times weekly. Target Hb is 11-12 g/dL and failure to respond may be the result of haematinic deficiency, bleeding, malignancy or infection. The disadvantages of treatment are that erythropoietin may accelerate hypertension and, rarely, lead to encephalopathy with convulsions.
Acidosis Systemic acidosis accompanies the decline in renal function and may contribute to increased serum potassium levels as well as dyspnoea and lethargy. Treatment is with oral sodium bicarbonate (4.8 g or 57 mmol daily).
Infections Patients with CKD have an increased risk of infections which may be fatal. Influenza and pneumococcal vaccination should be administered.
Referral to a nephrologist
Most patients with CKD are managed in primary care and do not require referral to a nephrologist at the outset. Indications for specialist referral are based on the need for further investigation, complex treatment or because there is a high likelihood of progression to dialysis (Table 9.16).
1. Ethics and communication
2. Infectious diseases
3. Gastroenterology and nutrition
4. Liver, biliary tract and pancreatic disease
Liver, biliary tract and pancreatic disease
LIVER BIOCHEMISTRY AND LIVER FUNCTION TESTS
SYMPTOMS AND SIGNS OF LIVER DISEASE
NON - ALCOHOLIC FATTY LIVER DISEASE (NAFLD)
COMPLICATIONS AND EFFECTS OF CIRRHOSIS
TYPES OF CHRONIC LIVER DISEASE AND CIRRHOSIS
PRIMARY SCLEROSING CHOLANGITIS
BUDD - CHIARI SYNDROME
LIVER DISEASE IN PREGNANCY
CARCINOMA OF THE PANCREAS
NEUROENDOCRINE TUMOURS OF THE PANCREAS
5. Haematological disease
Assessment and treatment of suspected neutropenic sepsis
INHERITED HAEMOLYTIC ANAEMIAS
ACQUIRED HAEMOLYTIC ANAEMIA
THE WHITE CELL
HAEMOSTASIS AND THROMBOSIS
6. Malignant disease
COMMON INVESTIGATIONS IN MUSCULOSKELETAL DISEASE
COMMON REGIONAL MUSCULOSKELETAL PROBLEMS
THE SERONEGATIVE SPONDYLOARTHROPATHIES
Clinical features, Investigations
INFECTION OF JOINTS AND BONES
AUTOIMMUNE RHEUMATIC DISEASES
SYSTEMIC INFLAMMATORY VASCULITIS
DISEASES OF BONE
8. Water, electrolytes and acid–base balance
WATER AND ELECTROLYTE REQUIREMENTS
BODY FLUID COMPARTMENTS
REGULATION OF BODY FLUID HOMEOSTASIS
PLASMA OSMOLALITY AND DISORDERS OF SODIUM REGULATION
DISORDERS OF POTASSIUM REGULATION
DISORDERS OF MAGNESIUM REGULATION
DISORDERS OF ACID - BASE BALANCE
9. Renal disease
INVESTIGATION OF RENAL DISEASE
URINARY TRACT INFECTION
HYPERTENSION AND THE KIDNEY
RENAL CALCULI AND NEPHROCALCINOSIS
URINARY TRACT OBSTRUCTION
ACUTE RENAL FAILURE/ACUTE KIDNEY INJURY
CHRONIC KIDNEY DISEASE
RENAL REPLACEMENT THERAPY
CYSTIC RENAL DISEASE
TUMOURS OF THE KIDNEY AND GENITOURINARY TRACT
DISEASES OF THE PROSTATE GLAND
10. Cardiovascular disease
COMMON PRESENTING SYMPTOMS OF HEART DISEASE
INVESTIGATIONS IN CARDIAC DISEASE
ISCHAEMIC HEART DISEASE
VALVULAR HEART DISEASE
PULMONARY HEART DISEASE
ARTERIAL AND VENOUS DISEASE
DRUGS FOR ARRHYTHMIAS
DRUGS FOR HEART FAILURE
DRUGS AFFECTING THE RENIN - ANGIOTENSIN SYSTEM
NITRATES, CALCIUM - CHANNEL BLOCKERS AND POTASSIUM - CHANNEL ACTIVATORS
11. Respiratory disease
12. Intensive care medicine
13. Drug therapy, poisoning, and alcohol misuse
14. Endocrine disease
PITUITARY HYPERSECRETION SYNDROMES
THE THYROID AXIS
MALE REPRODUCTION AND SEX
FEMALE REPRODUCTION AND SEX
THE GLUCOCORTICOID AXIS
THE THIRST AXIS
DISORDERS OF CALCIUM METABOLISM
DISORDERS OF PHOSPHATE CONCENTRATION
ENDOCRINOLOGY OF BLOOD PRESSURE CONTROL
DISORDERS OF TEMPERATURE REGULATION
15. Diabetes mellitus and other disorders of metabolism
16. The special senses
COMMON NEUROLOGICAL SYMPTOMS
COORDINATION OF MOVEMENT
THE CRANIAL NERVES
COMMON INVESTIGATIONS IN NEUROLOGICAL DISEASE
UNCONSCIOUSNESS AND COMA
STROKE AND CEREBROVASCULAR DISEASE
EPILEPSY AND LOSS OF CONSCIOUSNESS
NERVOUS SYSTEM INFECTION AND INFLAMMATION
HEADACHE, MIGRAINE AND FACIAL PAIN
SPINAL CORD DISEASE
DEGENERATIVE NEURONAL DISEASES
DISEASES OF THE PERIPHERAL NERVES