7
Renal Failure
Pramod Nagaraja and Farid Ghalli
Department of Nephrology and Transplantation, University Hospital of Wales, Cardiff, UK
Abstract
This chapter gives an introduction to the aetiology, assessment, and treatment of acute kidney injury, chronic kidney disease, and end‐stage renal disease. Acute kidney injury (AKI) is common in patients who are hospitalised and is associated with significant morbidity and mortality. Early recognition is crucial to improving outcomes. Pre‐emptive renal transplantation is the treatment of choice for end‐stage renal disease in patients who meet requirements.
Keywords: acute kidney injury (AKI); acute tubular necrosis; chronic kidney disease; dialysis; end‐stage renal disease
7.1 Acute Kidney Injury
7.1.1 Definition
Acute kidney injury (AKI, previously known as ‘acute renal failure’) is a condition in which a person has a rapid decline in kidney function over hours to days, leading to an accumulation of by‐products of metabolism and disturbances in fluid, acid–base balance, and electrolyte balance. It is defined as any one of the following: Increase in serum creatinine (SCr) by >0.3 mg dl−1 (>26.5 μmol l−1) within 48 hours, increase in SCr to >1.5 times baseline, which is known or presumed to have occurred within the last 7 days, or urine volume < 0.5 ml kg−1 h−1 for 6 hours [1, 2]. The AKI Network (AKIN) group and Kidney Disease: Improving Global Outcomes (KDIGO) developed the definition so that it redefines the entire spectrum of acute renal dysfunction to capture all patients with rises in SCr that are of clinical significance but may not result in complete failure of kidney function [1, 2].
7.1.2 Stages of AKI
AKI is classified as mild, moderate, or severe according to the degree of rise of serum creatinine and the urine output, as shown in Table 7.1. This method of grading AKI has been validated clinically by studies showing an increased risk of mortality with increasing severity of AKI (correcting for comorbidity) [3, 4].
Table 7.1 AKIN grading of acute kidney injury (AKI).
| Stage | Serum creatinine | Urine output |
| 1 | 1.5–1.9 times baseline Or ≥0.3 mg dl−1 (≥26.5 μmol l−1) increase | <0.5 ml kg−1 h−1 for 6–12 hours |
| 2 | 2.0–2.9 times baseline | <0.5 ml kg−1 h−1 for ≥12 hours |
| 3 | ≥3.0 times baseline Or SCr ≥4.0 mg dl−1 (≥353 μmol l−1) Or Initiation of renal replacement therapy | <0.3 ml kg−1 h−1 for ≥24 hours Or Anuria for ≥12 hours |
AKIN, Acute Kidney Injury Network.
7.1.3 Classification of AKI
AKI is classified based on aetiology into pre‐renal, renal (intrinsic), and post‐renal.
7.1.3.1 Prerenal AKI
This is usually as a result of a decrease in effective intra‐arterial volume due to haemorrhage or fluid losses. Renal arterial obstruction and intrarenal ischaemia as a result of various causes can also lead to prerenal AKI (Table 7.2). The hallmark of prerenal AKI is the reversibility of renal dysfunction without any structural damage to renal parenchyma, following treatment of the underlying prerenal cause.
Table 7.2 Prerenal causes of acute kidney injury (AKI).
| Volume loss Haemorrhage Vomiting and diarrhoea Diuresis without fluid replacement Burns Decreased Renal Perfusion Renal artery thrombus/embolus Renal artery stenosis Intrarenal ischaemia Congestive cardiac failure Systemic sepsis Hepatorenal syndrome Nephrotic syndrome Abdominal compartment syndrome Drug‐induced (NSAIDs, ACE‐i, CNI) |
ACE‐i, angiotensin‐converting enzyme‐inhibitor; CNI, calcineurin inhibitor; NSAIDs, nonsteroidal anti‐inflammatory drugs.
7.1.3.2 Intrinsic AKI
Renal parenchyma can be damaged by tubulointerstitial diseases, glomerular diseases, or vasculitis. Prerenal causes, if untreated or severe, can lead to acute tubular necrosis (ATN) which by far is the most common cause of AKI amongst patients in hospitals. A variety of small vessel inflammatory diseases can affect the kidney leading to AKI. Some of these aetiologies are shown in Table 7.3.
Table 7.3 Causes of intrinsic acute kidney injury (AKI).
| Small vessel diseases Microscopic polyangiitis Glomerulitis with polyangiitis (Wegener granulomatosis) Cryoglobulinaemia Haemolytic uraemic syndrome Thrombotic thrombocytopenic purpura Disseminated intravascular coagulation Cholesterol emboli Eclampsia Malignant hypertension Scleroderma Other glomerular diseases Anti‐glomerular basement membrane disease (Goodpasture syndrome) ANCA‐associated vasculitis Systemic lupus erythematosus (SLE) Postinfectious glomerulonephritis Henoch‐Schönlein purpura Tubulointerstitial nephritis and diseases Drug‐induced nephritis NSAIDs Antibiotics Proton pump inhibitors Drug toxicity Aminoglycosides Tenofovir Cisplatin Other toxins Radiocontrast media Myoglobin Immunoglobulin light chains Plant and mushroom toxins Crystals Urate Oxalate Acyclovir Granulomatous diseases Sarcoidosis Tubulointerstitial nephritis and uveitis (TUNI) syndrome Infection Acute bacterial pyelonephritis Malaria Leptospirosis |
ANCA, antineutrophil cytoplasmic antibodies; NSAIDs, nonsteroidal ant‐inflammatory drugs.
7.1.3.3 Postrenal or Obstructive AKI
The obstruction to urine flow can occur anywhere in the urinary tract, from the tubules, as a result of crystal nephropathy, down to the prostate. Common causes of obstructive AKI are shown in Table 7.4.
Table 7.4 Causes of obstructive acute kidney injury (AKI).
| Intrinsic to the tract Calculi Blood clots Crystals Malignancy Ureteric strictures Postradiation fibrosis Prostatic diseases Extrinsic to the tract Pelvic malignancy including lymphadenopathy Retroperitoneal fibrosis Iatrogenic ureteric injury |
7.1.4 Clinical Assessment
A thorough clinical assessment is essential to differentiate AKI from chronic kidney disease and to identify the aetiology and mechanism of AKI. This includes the clinical history that can point towards prerenal AKI in the presence of gastrointestinal fluid losses, systemic sepsis, and so on. Medication history is important because a variety of drugs can cause prerenal AKI and allergic interstitial nephritis. Many causes of intrinsic AKI (e.g. vasculitis, sarcoidosis, and systemic lupus erythematosus) may be associated with systemic symptoms such as fever, arthralgia, and fatigue. Lower urinary tract symptoms or a history of pelvic malignancy may suggest an obstructive cause.
Physical examination should focus on assessing volume status (i.e. heart rate, blood pressure, jugular venous pressure, skin turgor, presence of oedema, or lung crackles) and identifying sepsis early. Rash, arthritis, or red eyes may suggest vasculitis. Pelvic examination to look for enlarged bladder, prostatic enlargement, and gynaecological malignancy is essential in the presence of relevant symptoms.
Bedside urine dipstick examination is mandatory. Haematuria and proteinuria are present in glomerulonephritis. Leucocytes and nitrites suggest infection. Eosinophiluria may be present in allergic interstitial nephritis.
7.1.4.1 Investigations
It is essential that the diagnosis of AKI and its possible cause be identified as a matter of urgency to prevent irreversible damage or to limit damage. In addition to elevated serum urea and creatinine, there may be metabolic acidosis and hyperkalaemia. Hypercalcaemia and hyperuricaemia must be ruled out as possible causes of AKI. Full blood count, C‐reactive protein (CRP), and blood cultures are essential to identify sepsis.
Further investigations are directed towards answering two important questions: Is urinary obstruction a possibility and is intrinsic AKI or systemic disease a possibility? Therefore, all patients with suspected or confirmed AKI must have a renal tract ultrasound as soon as possible. If intrinsic AKI is considered, then the following tests must be done: antinuclear antibodies (ANA), antineutrophil cytoplasmic antibodies (ANCA), anti‐GBM antibodies, myeloma screen, and complement C3 and C4 levels. Blood film examination, serum lactate dehydrogenase (LDH), and haptoglobin levels are useful if haemolytic uraemic syndrome (HUS) or thrombotic thrombocytopenic purpura (TTP) are suspected.
Indications for performing a renal biopsy for AKI include: (i) unclear cause for AKI, (ii) delayed recovery from presumed ATN, (iii) suspected systemic disease with renal involvement, and (iv) suspected glomerulonephritis.
Several novel biomarkers for AKI have been identified in recent years, including kidney injury molecule‐1 (KIM‐1), neutrophil gelatinase associated lipocalin (NGAL), interleukin‐18 (IL‐18), and cystatin C. However, these tests are not yet widely used in clinical practice, and they remain the focus of ongoing studies to determine their appropriate role in guiding management of patients at risk for AKI.
7.1.5 Management
7.1.5.1 Early Nephrology Consultation
Early nephrology referral is recommended because a delay in referral has been associated with increased morbidity and mortality, dialysis dependence, and prolonged hospital stay in patients who are critically ill with AKI [5, 6]. Referral is especially recommended in a timely manner in the following situations:
- Dialysis indications exist
- Unexplained cause and deteriorating AKI
- Possible glomerulonephritis
- Possible autoimmune disease
- Possible pulmonary‐renal syndrome
- Possible HUS or TTP
7.1.5.2 Correction of Prerenal States and Maintenance of Haemodynamic Stability
In the absence of haemorrhagic shock, KDIGO guidelines suggest using isotonic crystalloids (physiological saline) rather than colloids (albumin or starches) as initial management for expanding the intravascular volume in patients at risk for AKI or with AKI. Patients with vasomotor shock will need to be cared for in a high‐dependency setting with the use of vasopressors. Accurate and regular fluid balance monitoring is crucial to avoid volume overload and pulmonary oedema, especially in patients with oliguria. In established ATN, the focus of management should be towards preventing complications of AKI and maintaining a physiological environment that aids recovery of renal function. Sepsis should be identified and treated early.
7.1.5.3 Treatment of Complications
Hyperkalaemia is a common and dangerous complication in patients with AKI. If serum potassium level is >6 mmol l−1, then an electrocardiogram (ECG) must be undertaken to check for features of hyperkalaemia, and if present, then calcium gluconate is given to stabilise the cardiac cell membrane and prevent arrhythmias. Serum potassium level can be decreased by giving glucose and insulin intravenously (IV) or salbutamol nebulisers. Correction of acidosis with sodium bicarbonate given IV or orally also helps in correcting hyperkalaemia. Hypocalcaemia and hyponatraemia are also common problems in patients with AKI that will need correcting. AKI can also lead to a bleeding tendency because of platelet dysfunction and the presence of sepsis; dialysis may be required to improve this.
7.1.5.4 Medication Management
Nephrotoxic agents such as aminoglycosides, nonsteroidal anti‐inflammatory drugs (NSAIDs), angiotensin‐converting enzyme‐inhibitor (ACE‐i), and angiotensin receptor blockers (ARBs) must be avoided or stopped. Doses of certain medications may need adjusting in the presence of AKI to avoid the risk of accumulation and toxicity.
7.1.5.5 Other Supportive Care
Good nutritional support is crucial during recovery from AKI. KDIGO guidelines suggest achieving a total energy intake of 20–30 kcal kg−1 day−1 in patients with any stage of AKI and protein intake of 0.8–1.0 g kg−1 day−1 in noncatabolic patients with AKI not requiring dialysis. A higher protein intake of 1.0–1.5 g kg−1 day−1 is recommended in patients with AKI on dialysis. Nutrition is given preferentially via the enteral route.
Diuretics are not recommended for the prevention or treatment of AKI, except in the management of volume overload. Diuretics are helpful in managing cardiac failure and cirrhosis in patients with AKI when used in conjunction with other measures to improve the underlying haemodynamics.
7.1.5.6 Renal Replacement Therapy
In some patients, the AKI is severe enough to require renal replacement therapy (RRT). Usual indications for initiating dialysis in AKI are as follows
- Resistant hyperkalaemia
- Resistant acidosis (e.g. pH < 7.2)
- Pulmonary oedema unresponsive to diuretics
- Uraemic encephalopathy
- Uraemic pericarditis
In patients with haemodynamic instability, continuous renal replacement therapy (CRRT; e.g. continuous veno‐venous haemofiltration [CVVHF]) is preferred. In most cases, however, intermittent haemodialysis (HD) is given. Because HD is likely to be temporary, this is undertaken using a double‐lumen catheter inserted into the jugular or femoral veins. Anticoagulation in the form of heparin is usually necessary to prevent clotting of blood within the dialysis circuit. This significantly adds to the bleeding risk in patients with AKI and must be taken into consideration when surgical, radiological, or vascular interventions are also needed.
Recovery from ATN may take up to 6 weeks but sometimes as long as 12 weeks. Dialysis dependence for longer than 12 weeks would be classified as end‐stage renal disease (ESRD).
7.2 Chronic Kidney Disease
Chronic kidney disease (CKD) is defined as abnormalities of kidney structure or function, present for more than three months with adverse implications for health [7]. The abnormalities may be structural (detected by imaging), histological (biopsy findings), or electrolyte disturbances. KDIGO has classified CKD based on the glomerular filtration rate (GFR) and the amount of albuminuria. This categorisation also defines the risk of progression of CKD towards ESRD needing RRT (Figure 7.1). CKD and its complications significantly increase the risk of cardiovascular disease.
Figure 7.1 Classification and prognosis of chronic kidney disease (CKD).
Source: From [7].
Although SCr level is used routinely as a marker of renal function, SCr is affected by a number of other factors such as age, gender, race, nutritional state, and diet. Therefore, various equations have been developed to estimate the GFR. Two widely used equations are the Modification of Diet in Renal Disease (MDRD) formula [8] and the Chronic Kidney Disease Epidemiology (CKD‐Epi) formula [9]. The CKD‐Epi formula is more accurate than the MDRD, especially in subjects with preserved GFR levels.
Common causes of CKD and ESRD include diabetes mellitus, hypertension, glomerulonephritis, cystic renal diseases, and pyelonephritis. The prevalence of CKD stages three to five increases with age. One population‐based study in the UK estimated the prevalence in adults ages 45–54 as approximately 3.5% and in adults ages 75–84 as approximately 35% [10].
7.2.1 Clinical Assessment
Initial clinical assessment for CKD includes a search for the possible cause to offer specific treatment (e.g. immunosuppression therapy for some types of glomerulonephritis and relieving urinary obstruction). When no specific treatment exists, then the main aim of managing CKD would be to reduce the risk of CKD progression and managing associated complications such as cardiovascular disease, anaemia, metabolic acidosis, mineral bone disorders, and the risk of AKI. Patients with stage 5 CKD and those needing RRT are said have ESRD.
7.2.2 Complications and Their Management
7.2.2.1 Volume Overload
Extracellular volume expansion and total‐body volume overload results from failure of sodium and free‐water excretion. This generally becomes clinically manifested when the GFR falls to less than 20 ml min−1, although this may occur with higher GFR in patients with diabetes. Loop diuretics are generally necessary to manage fluid volume expansion and blood pressure control in CKD. Reducing salt and fluid consumption in the diet is also essential.
7.2.2.2 Electrolyte and Acid–Base Imbalances
Hyperkalaemia usually does not develop until the GFR falls to less than 20 ml min−1. This especially occurs in patients who ingest a potassium‐rich diet, diabetics and those on ACE‐i, NSAIDs, or beta‐blockers. Treatment is with a low‐potassium diet, diuretics, potassium‐binding resins, and reducing or stopping ACE‐i and ARBs in the short term.
Metabolic acidosis often is a mixture of normal anion gap and increased anion gap. Treatment of acidosis with sodium bicarbonate is necessary to manage hyperkalaemia effectively.
7.2.2.3 Skin Manifestations
Itching can be a distressing feature of renal failure. The pathophysiology is still unclear. Anaemia, iron deficiency, hyperphosphataemia, and hyperparathyroidism may all contribute to itching. If treating these conditions does not help with the symptoms, then antihistamines or gabapentin could be tried [11].
7.2.2.4 Anaemia
Anaemia is common in patients with CKD, especially after the GFR falls to <30 ml min−1. Once other causes of anaemia have been ruled out (e.g. bone marrow and gastrointestinal disease), then the treatment focuses on correction of iron, vitamin B12 and folic acid deficiency and erythropoiesis‐stimulating agents (ESAs) [12]. Intravenous iron is frequently required. ESAs are given as subcutaneous injection on a weekly to monthly basis and in patients on HD, it is usually given IV. The aim is to maintain a haemoglobin level between 10 and 12 g l−1.
7.2.2.5 Neurologic Manifestations
Peripheral neuropathy can occur in ESRD resulting in paraesthesiae, weakness and loss of sensation, most marked in the feet. This is mostly irreversible in severe cases but adequate dialysis treatment and renal transplantation usually helps. Tricyclic antidepressants and gabapentin are used for neuropathic pain with variable effect. Quinine sulphate and clonazepam can be used for restless legs.
Mental changes such as decreased memory and concentration, slow and slurred speech, myotonic jerks, seizures, altered smell and taste, and sleep disturbances are manifestations of advanced uraemia which indicates the necessity of dialysis.
7.2.2.6 Hypertension
Hypertension (HTN) is a common complication of renal impairment from any cause. Also, HTN is a major risk factor for progressive CKD. Therefore, controlling HTN is major goal in patients with kidney disease. The target blood pressure depends on whether or not proteinuria is present, which is also a risk factor for progressive CKD. In ESRD, HTN is usually driven by fluid volume overload, and therefore controlling fluid volume by dietary means and dialysis is crucial.
7.2.2.7 Mineral Bone Disease
Reduction of renal cell mass leads to progressive phosphate retention and failure of renal bioactivation of vitamin D by 1‐alpha hydroxylase, with consequent hyperphosphataemia and relative hypocalcaemia. This stimulates an increased production of parathormone, leading to secondary hyperparathyroidism. Ultimately, tertiary hyperparathyroidism can develop where there is failure of the negative feedback mechanism. Adverse consequences of mineral bone disease include vascular calcification, calciphylaxis, resistant pruritus, and anaemia. Correction of these abnormalities require adequate dialysis, gut phosphate binders, and activated vitamin D. Tertiary hyperparathyroidism may need cinacalcet (a calcimimetic agent acting on the parathyroid gland) or parathyroidectomy.
7.2.2.8 Amyloidosis
Beta 2‐microglobulin amyloidosis is a disabling condition that affects patients undergoing long‐term HD or peritoneal dialysis (PD). It is mainly prevalent in patients who have been on dialysis for a long time (5–10 years). It manifests as pain due to carpal tunnel syndrome, joint capsulitis, arthritis, and bone cysts. More effective dialysis therapies and renal transplantation in recent years is expected to reduce the prevalence of this condition by better clearing beta 2‐microglobulin from the blood.
7.2.2.9 Other Uraemic Features
- Constitutional: fatigue, generalised weakness, muscle cramps, restless legs
- Gastrointestinal: anorexia, nausea and vomiting, gastritis
- Pericarditis: potentially lethal complication of uraemia, which if present is an indication for urgent dialysis
- Haematologic: platelet dysfunction and bleeding
- Sexual: amenorrhea, infertility, impotence
7.2.3 Renal Replacement Therapy
Kidney transplantation is the treatment of choice for ESRD in suitable patients because it improves both the survival and the quality of life (QoL) compared to dialysis. Transplantation before the initiation of dialysis (pre‐emptive transplantation) should be the aim as it offers the best outcomes in terms of survival and QoL. Unfortunately, owing to comorbidities, only around 30% of patients who develop ESRD are fit enough to be listed for transplantation. Renal transplantation is covered in greater detail in a separate chapter.
Residual renal function is important in patients starting dialysis. This is especially so for patients because small solute removal is not very good with PD, and maintaining fluid balance will be challenging when the daily urine output is less than 0.5 l. Therefore, nephron‐sparing surgery is crucial in the right context. In patients on HD, because residual renal function usually declines significantly within a few months after starting dialysis, salt and fluid restriction in the diet are extremely important in managing fluid balance and blood pressure.
Patients with ESRD have a poorer QoL than the general population [13] but there is no evidence that dialysis or transplantation improves QoL significantly. However, patients who have undergone transplants have been shown to have a better QoL than those on either HD or PD [14]. It is still not clear if there is difference between HD and PD in terms of QoL improvement [14, 15], and therefore, treatment choices have to be individualised after appropriate education of patients with ESRD.
Patients with ESRD, even those who are on RRT, have a higher mortality compared to age‐matched general population. There are wide global variations in survival rates of dialysis patients, which is thought to reflect variations in life expectancies and dialysis practices [16]. Survival is also influenced significantly by age. For example, in the UK, the median survival time of incident haemodialysis patients is approximately 10 years for adults ages 45–54 compared to 3.5 years for adults ages 65–74 [17]. The main causes of death are cardiovascular, infection, and withdrawal from dialysis. There are conflicting reports from mainly observational and retrospective studies indicating the lack of a long‐term survival advantage of PD over HD.
Dialysate fluid buffers.
7.3 Dialysis
7.3.1 Peritoneal Dialysis
PD is a home‐based mode of RRT, which gives a degree of flexibility and control to patients with ESRD in terms of lifestyle. A PD catheter made of silicone or polyurethane placed in the abdominal cavity is an essential requirement for undertaking PD. The PD catheter is inserted into the abdomen under local or general anaesthetic. Medical percutaneous approach, open surgical approach, and laparoscopic method are all used for this purpose depending on local expertise and practice. The tip of the catheter should lie in the pelvic cavity (Figure 7.2). Dacron cuffs on the catheter elicit a fibrous reaction which anchor the catheter to the abdominal wall and help to prevent infection. The catheter is tunnelled subcutaneously to exit the skin at an appropriate site. There has been no demonstrable differences in outcomes between insertion techniques or different types of modern PD catheters [18]. Although PD can be started immediately after insertion of the catheter, it is usually started after a period of two to four weeks to allow wound healing and to reduce the risk of leak of dialysate from around the catheter [19, 20].
Figure 7.2 A catheter is placed in the pelvis and 2 l quantities of dialysate are run into the peritoneal cavity, left for four to six hours, and run out again.
Absolute contraindications to PD include diaphragmatic defects, peritoneal adhesions, surgically uncorrectable abdominal hernias, and acute ischaemic or infectious bowel disease. Relative contraindications include severe obesity, lack of manual dexterity, abdominal stomas, dementia, and poor personal hygiene.
In PD, the peritoneal membrane acts as a semi‐permeable membrane across which solute and water move between the vascular compartment and the peritoneal cavity. PD fluid contains sodium, chloride, calcium, magnesium, water, and a variable concentration of glucose. Bicarbonate or lactate act as buffers. Clearance of uraemic toxins occurs by way of diffusion down a concentration gradient and by convection. The high glucose content in the dialysate exerts an osmotic gradient which helps in moving water from the vascular compartment into the peritoneal cavity and ultimately out of the patient.
In its simplest form, PD is a manual procedure where the patient is taught to perform dialysis exchanges three to four times a day using a sterile technique (continuous ambulatory PD [CAPD]). Here, 2 l of the dialysate is inserted into the abdominal cavity using the PD catheter, allowed to dwell for four to six hours and then drained out, with a fresh volume of dialysate inserted again. Automated PD (APD) or continuous cycling PD (CCPD) is an alternative to CAPD where several exchanges are performed overnight using a machine while the patient sleeps. This is a lifestyle choice for certain patients. However, APD offers other possible advantages such as increasing the dialysis dose and improving water removal. Modern APD machines are relatively small, portable, and easy to use.
7.3.1.1 Complications Associated with PD
- Drainage problems can occur due to migration of the catheter, so that the tip no longer lies in the pelvis (usually due to constipation). The catheter tip could also get blocked with fibrin, clot, or omentum. Management is by relieving constipation and using urokinase or heparin in the catheter. Repositioning or replacement of the catheter may be required.
- Leak of fluid from the peritoneal space may occur into various locations (e.g. anterior abdominal wall, inguinal hernia, or pleural space). Leaks are managed by withholding PD and repair of any hernias. Pleural leaks may need cessation of PD and switching to HD.
- Pain on inflow of fluid may mean that the catheter is not correctly placed in the peritoneal cavity or that the acidity of the fluid is high. It is usually transient. In persistent cases, using less acidic dialysate, incomplete drainage of fluid, slowing the rate of infusion, and catheter replacement are tried.
- Perforation of the bowel is rare and is most commonly associated with insertion, although slow perforation can also occur as a result of bowel wall erosion. Operative treatment is usually required.
- Infections associated with PD cause significant morbidity and mortality [21]. Exit site and tunnel infections are caused mainly by Staphylococcus aureus and Pseudomonas species. These have to be treated aggressively because they could lead to peritonitis. PD‐related peritonitis is a serious complication which can become life‐threatening, but could also lead to membrane failure. It presents with a cloudy effluent, fever, abdominal pain, or diarrhoea. Empirical treatment should cover both gram‐positive and ‐negative organisms. Severe and recurrent peritonitis or those caused by fungi require removal of the PD catheter.
- Encapsulating peritoneal sclerosis (EPS) is a rare but serious complication of PD whose risk increases with time spent on PD. Clinical manifestations include symptoms associated with bowel obstruction, hemoperitoneum, abdominal mass, and malnutrition. It occurs because of fibrosis of the peritoneum leading to ‘cocooning’ of small bowel. Treatment focuses on maintaining nutrition which may need to be parenteral. Surgical treatment may involve bowel resection and peritonectomy which are associated with a substantial mortality risk [22].
7.3.2 Haemodialysis
7.3.2.1 Principles
Blood from the patient flows through an extracorporeal circulation over a thin semi‐permeable membrane separating it from the dialysate fluid (Figure 7.3). The membrane is usually made of a synthetic material such as polysulfone. A modern dialyser unit (‘the artificial kidney’) is designed in the form of numerous tiny hollow tubes made using the membrane. Blood flows through these tubes with the dialysate fluid flowing in the opposite direction around the tubes (countercurrent flow). During this process, there is diffusion of solutes from the blood into the dialysate and vice versa, depending on concentration gradients Water removal occurs because of a pressure gradient applied across the membrane (ultrafiltration). Along with the water, convection of solutes, including small‐ to medium‐sized proteins, also occurs. The spent dialysate is discarded and blood is returned back to the patient.
Figure 7.3 Principle of haemodialysis: blood flows over a thin semi‐permeable membrane which separates it from the dialysis fluid.
Outpatient HD for ESRD is typically provided intermittently three times a week with a minimum of four hours each session. Daily HD can also be undertaken by patients in their own homes and for longer periods (six hours) including the night (nocturnal HD). Although longer and more frequent dialysis improves certain surrogate markers such as blood pressure and hyperphosphataemia, there is no strong evidence of improved mortality; in fact, there is some evidence of increased infectious and access complications associated with frequent HD [23–25].
Relative contraindications to HD include haemodynamic instability, severe heart failure, and inability to cooperate with the procedure.
7.3.2.2 Vascular Access
The chief problem in HD is a well‐functioning vascular access. Blood flow rates of 200–500 ml min−1 is required in the extracorporeal circulation. To achieve this, the best method is to create a peripheral arteriovenous fistula (AVF; e.g. radiocephalic or brachiocephalic). If this is not possible because of the size of the vessels, then an arteriovenous graft (AVG) is implanted. Four to six weeks are required for the draining vein of an AVF to arterialise and be suitable for needling. An AVG can be used much sooner after its creation. Two needles are inserted into an AVF or AVG to obtain blood and return purified blood. The least preferred option for access would be a tunnelled central venous catheter because it is associated with a high risk of infection, thrombosis and central venous stenosis.
7.3.2.3 Complications of HD
- Haemorrhage can occur through incorrect management of needles at the time of dialysis.
- Intradialytic hypotension manifests as dizziness, nausea, cramps, headache, and fainting. Slowing down the rate of fluid removal and intravenous fluid infusion may be required.
- Dialysis disequilibrium syndrome (DDS) is a rare complication, which occurs in patients with severe uraemia who have been subjected to aggressive dialysis initiation. Rapid reductions in serum osmolality and paradoxical cerebrospinal fluid acidosis results in cerebral oedema. Symptoms include restlessness, headache, tremors and occasionally fits, and coma occurring during or after dialysis. Short initial treatment using dialysers of small surface area and low blood pump settings prevent this problem.
- Complications of AVF or AVG include aneurysm formation, stenosis, infection, haematomas, and steal syndrome.
- Complications of central venous catheters include bacteraemia, thrombosis, venous stenosis, and malfunction necessitating replacements.
- High output cardiac failure is a rare complication. Like the arterial steal, it can usually be corrected by reversing the fistula.
Practice notes with patients on HD:
- Blood electrolyte levels take one to two hours to stabilise after a dialysis session, and therefore, caution is necessary whilst interpreting them.
- Some medications are removed by dialysis, and therefore, should be given at the end of a dialysis session. Always consult a renal pharmacist.
- If major surgery is planned, it will be beneficial to dialyse the day before to optimise fluid and electrolyte status and transfuse blood products if necessary.
- There is an increased risk of renal cancer in patients with ESRD on HD.
- There is an increased risk of bleeding in patients on HD due to the use of anticoagulation of the dialysis circuit. This should be taken into account while planning invasive procedures.
7.3.3 Continuous Renal Replacement Therapies (CRRT)
CRRT is used in intensive care units (ICUs) in patients who are critically ill with AKI, especially in those with haemodynamic instability in whom it is preferred over intermittent HD. It is intended to be used continuously over a 24‐hour period using double‐lumen venous dialysis catheter. Solute removal during CRRT is achieved by convection (haemofiltration), diffusion (HD), or a combination of both the methods (haemodiafiltration). Middle and larger molecular‐weight substances are more efficiently removed using haemofiltration as compared to HD. During haemofiltration, negative pressure applied across a semi‐permeable membrane causes fluid movement away from blood. Solutes are dragged across the membrane with the fluid resulting in convective transport of solutes away from the blood. This process requires the use of a replacement fluid to replace fluid and electrolytes back into the patient to prevent excessive fluid removal and electrolyte imbalance. Haemodiafiltration combines diffusive and convective methods to improve clearance of both small and large molecular‐weight substances. Similar to HD, anticoagulation is needed to prevent clotting of the extracorporeal circuit. This is achieved by either heparin or increasingly using regional citrate infusion.
7.3.4 Conservative Management
Maximal conservative management (MCM) is the support of patients with ESRD without resorting to RRT in the form of dialysis or transplantation [26]. This support addresses the patient’s physical, emotional, and spiritual needs until the end of life. Nondialytic therapy includes the treatment of renal anaemia with erythropoietin, optimization of fluid balance with diuretics, and symptomatic treatment of uraemic symptoms such as nausea, itching, and pain. There are some data to suggest that selected elderly patients with high extrarenal comorbidity live just as long with MCM as with dialysis [27]. The collective decision to pursue nondialytic therapy is reached after discussion amongst the patient, their families, and the healthcare team. Palliative care teams need to be closely involved in this approach, especially in planning end‐of‐life care.
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