ABC of Kidney Disease E-Book
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- Herausgeber: John Wiley & Sons
- Kategorie: Fachliteratur
- Serie: ABC Series
- Sprache: Englisch
ABC of Kidney Disease
ABC of Kidney Disease, Second Edition
The ABC of Kidney Disease, Second Edition is a practical guide to the most common renal diseases to help healthcare professionals screen, identify, treat and refer renal patients appropriately and to provide the best possible care.
Covering the common renal presentations in primary care, this highly illustrated guide provides guidance on symptoms, signs and treatments, which tests to use, measures to prevent progression, and when and how to refer. Fully revised in accordance with current guidelines, it also includes organizational aspects of renal disease management, dialysis and transplantation. The appendices contain an explanatory glossary of renal terms, guidance on anaemia management and information on drug prescribing and interactions.
The ABC of Kidney Disease, Second Edition is an ideal practical reference for GPs, GP registrars, junior doctors, medical students and for anyone working with patients with renal-related conditions.
About the ABC series
The new ABC series has been thoroughly updated, offering a fresh look, layout and features throughout, helping you to access information and deliver the best patient care. The newly designed books remain an essential reference tool for GPs, GP registrars, junior doctors and those in primary care, designed to address the concerns of general practitioners and provide effective study aids for doctors in training.
Now offering over 70 titles, this extensive series provides you with a quick and dependable reference on a range of topics in all the major specialities. Each book in the new series now offers links to further information and articles, and a new dedicated website provides you with even more support.
The ABC series is the essential and dependable source of up-to-date information for all practitioners and students in general practice.
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Seitenzahl: 265
Veröffentlichungsjahr: 2013
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Table of Contents
Series Page
Title page
Contributors
Preface
Chapter 1: Diagnostic Tests in Chronic Kidney Disease
Urine Testing
Non-visible Haematuria
Microalbuminuria and Proteinuria
Tests of Kidney Function
Renal Imaging
Renal Biopsy
Further Reading
Chapter 2: Acute Kidney Injury (Formerly Known as Acute Renal Failure)
Definition and Classification
Pre-renal Acute Kidney Injury
Intrinsic Renal Acute Kidney Injury
Post-renal Acute Kidney Injury
Prevention
Differential Diagnosis
Investigations
Management Principles
Summary
Further Reading
Chapter 3: Prevalence, Detection, Evaluation and Management of Chronic Kidney Disease
Introduction
Prevalence and Staging of Chronic Kidney Disease
Detection
Evaluation
Creatinine/Estimated Glomerular Filtration Rate
Albuminuria/Proteinuria (also See Chapter 1)
Haematuria (also See Chapter 1)
Renal Imaging (also See Chapter 1)
More Specialist/Other Renal Screening Tests for Underlying Cause of Chronic Kidney Disease
Management
References
Chapter 4: Pre-Dialysis Clinics: Preparing for End-Stage Renal Disease
Education
Preservation of Existing Renal Function and Reduction of Cardiovascular Risk Factors
Addressing Complications of Chronic Kidney Disease
Planning for End-stage Renal Failure
Additional Care Given in Low Clearance Clinics
Further Reading
Chapter 5: Anaemia Management in Chronic Kidney Disease
Prevalence and Impact of Anaemia of Chronic Kidney Disease
Causes
Previous Management Practices
Current Management
The Role of Care in the Community
References
Chapter 6: Urinary Tract Infections, Renal Stones, Renal Cysts and Tumours and Pregnancy in Chronic Kidney Disease
Urinary Tract Infections in Adults
Kidney Stones (Nephrolithiasis)
Renal Cysts and Tumours
Autosomal Dominant Polycystic Kidney Disease
Pregnancy in Chronic Kidney Disease
Further Reading
Chapter 7: Adult Nephrotic Syndrome
Nephrotic Syndrome
Conditions Causing Nephrotic Syndrome
The Pathophysiological Reasons for Nephrotic Syndrome
Explanations for Oedema in Nephrotic Syndrome
Complications of Nephrotic Syndrome
Assessing the Patient Presenting with Nephrotic Syndrome
Investigations
General Treatment Measures for Nephrotic Syndrome
Management of Primary and Secondary Glomerular Diseases Causing Nephrotic Syndrome
Conclusions
References
Further Resources
Chapter 8: Renal Artery Stenosis
Definition and Background
Clinical Features
Pathogenesis of Renal Dysfunction in Patients with Renal Artery Stenosis
Investigations
Management of Renal Artery Stenosis
Medical Treatment
Renal Revascularization
Prognosis of Patients with Atheromatous Renovascular Disease
Further Reading
Chapter 9: Palliative Care for Patients with Chronic Kidney Disease
Introduction
Which Renal Patients Need Palliative Care?
The Extent of the Clinical Need
Conservative Management of Patients Choosing not to Dialyse
Withdrawal from Dialysis
Symptoms: Identification and Control
Advanced Planning
Links with Palliative Care Services
Conclusions
References
Further Reading
Chapter 10: Dialysis
Introduction
Indications for Starting Renal Replacement Therapy
Preparation for Renal Replacement Therapy
Renal Replacement Therapy
Monitoring Adequacy of Renal Replacement Therapy
Developments in Delivery of Renal Replacement Therapy
Further Reading
Chapter 11: Renal Transplantation
Introduction
Immunological Aspects of Transplantation
The Kidney Donor
Recipient
Bladder Function
Surgical Aspects
Post-operative Management
Immunosuppression
Complications
Rejection
Chronic Allograft Nephropathy
Infection
Malignancy
Recurrence
Outcome
The Future
Further Reading
Chapter 12: Chronic Kidney Disease, Dialysis and Transplantation in Children
Introduction
Structural Abnormalities of the Kidneys and Urinary Tract
Polycystic Kidney Disease
Inherited, Tubular and Metabolic Diseases
Idiopathic Childhood Nephrotic Syndrome
Glomerulonephritis in Children
Chronic Kidney Disease
Renal Replacement Therapy
Further Reading
Chapter 13: The Organization of Services for People with Chronic Kidney Disease: A 21st-Century Challenge
Introduction
The 2007 Model of Service
Challenges for Renal Health Care
The Roles of Primary Care
Planning for Renal Replacement Therapy
Dialysis and Transplantation
Independent Sector Treatment Centres
Supportive and Palliative Care in Chronic Kidney Disease
Current Developments (See Appendix 4)
Conclusion
References
Further Reading
Appendix 1: Chronic Kidney Disease and Drug Prescribing
Pain Management in Patients with Chronic Kidney Disease
Prescribing for Patients with Chronic Kidney Disease/End Stage Renal Failure
Further Resources
Appendix 2: Glossary of Renal Terms and Conditions
Alport's Syndrome
Anti-GBM (Goodpasture's) Disease
Autosomal Dominant Polycystic Kidney Disease
Diabetic Nephropathy (DN)
Focal Segmental Glomerulosclerosis
Glomerulonephritis
IgA disease and Henoch–Schönlein Purpura
Interstitial Nephritis
Lupus Nephritis
Membranous Nephropathy
Minimal Change Nephropathy
Myeloma, Amyloid and the Kidney
Nephrotic Syndrome
Pyelonephritis
Renal (ANCA-positive) Vasculitis
Renovascular Disease
Thin Membrane Nephropathy
Appendix 3: Top Ten Tips in Kidney Disease
1 Acute Screen
2 Hyperkalaemia
3 Contrast Nephrotoxicity (CN)
4 Starting an ACE Inhibitor +/−ARB
5 Change in GFR
6 Proteinuria
7 Sudden Onset of Heavy Proteinuria
8 Haematuria (Visible or Non-visible)
9 Correcting eGFR for Race
10 Non-diabetic Renal Disease
Appendix 4: Maps Showing Variation in Healthcare for People with Kidney Disease
Figure A4.1 Rate of RRT per population by country (2009; for 6 of the countries, data are not 2009)
Figure A4.2 Proportion (%) of people starting RRT for CKD <90 days after presenting to renal services by renal centre (2009)
Figure A4.3 Percentage of patients on the CKD register in whom the last blood-pressure reading, measured in the preceding 15 months, is 140/85 mmHg or less by PCT (2010/11)
Figure A4.4 Percentage of patients with diabetes with a diagnosis of proteinuria or micro-albuminuria who are treated with ACEIs (or A2 antagonists) by PCT (2010/11)
Index
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Contributors
Preface
This is the second edition of this popular handbook on kidney disease. It is necessary because important advances have been made in several areas, including the treatment of the anaemia associated with chronic kidney disease. Moreover, with the passage of time, more is now known about the prevalence, and importance, of chronic kidney disease in the United Kingdom and the rest of the world. In this second edition, we refine the presentation of the information concerning chronic kidney disease, we expand on the importance of good preparation for dialysis and transplantation, where those options are relevant, and we expand on the important area of conservative, or non-dialytic, management of the symptoms of chronic kidney disease, an option which is taken by increasing numbers. We have also revised the appendices, which include a Top Ten Tips section for quick reference. All in all, we hope and feel that this new version is an improvement on its predecessor, and that readers (from students to non-kidney specialists) will find this book a useful guide to the best management of a growing number of patients.
Chapter 1
Diagnostic Tests in Chronic Kidney Disease
Behdad Afzali1, Satish Jayawardene2 and David Goldsmith1
1King's College London, London, UK
2King's College Hospital NHS Foundation Trust, London, UK
Symptoms of chronic kidney disease (CKD) are often non-specific (Table 1.1). Clinical signs (of CKD, or of systemic diseases or syndromes) may be present and recognized early on in the natural history of kidney disease but, more often, both symptoms and signs are only present and recognized very late—sometimes too late to permit effective treatment in time to prepare for dialysis. However, the most commonly performed test of renal function—plasma creatinine—is typically performed with every hospital inpatient and as part of investigations or screening during many GP surgery or hospital clinic outpatient episodes.
Table 1.1 Signs and symptoms of chronic kidney disease
Symptoms
Signs
Tiredness
Pallor
Anorexia
Leuconychia
Nausea and vomiting
Peripheral oedema
Itching
Pleural effusion
Nocturia, frequency, oliguria
Pulmonary oedema
Haematuria
Raised blood pressure
Frothy urine
Loin pain
Unlike ‘angina’ or ‘chronic obstructive airways disease’, where a history can be revealing (e.g. walking distance or cough), there is little that is quantifiable about CKD severity without blood and/or urine testing.
This is why serendipitous discovery of kidney problems (haematuria, proteinuria, structural abnormalities on kidney imaging or loss of kidney function) is a common ‘presentation’. A full understanding of what these abnormalities mean and a clear guide to ‘what to do next’ are particularly needed in kidney medicine, and filling this gap is one of the aims of this book.
Correct use and interpretation of urine dipsticks and plasma creatinine values (by far the commonest tests used for screening and identification of kidney disease) is the main focus of this chapter. Renal imaging and renal biopsy will also be described briefly.
Urine Testing
Urinalysis is a basic test for the presence and severity of kidney disease. Testing urine during the menstrual period in women, and within 2–3 days of heavy strenuous exercise in both genders, should be avoided, to avoid contamination or artefacts. Fresh ‘mid-stream’ urine is best, again to reduce accidental contamination. Refrigeration of urine at temperatures from +2 to +8°C assists preservation. Specimens that have languished in an overstretched hospital laboratory specimen reception area, before eventually undergoing analysis, will rarely reveal all of the potential information that could have been gained.
Changes in urine colour are usually noticed by patients. Table 1.2 shows the main causes of different-coloured urine. Chemical parameters of the urine that can be detected using dipsticks include urine pH, haemoglobin, glucose, protein, leucocyte esterase, nitrites and ketones. Figure 1.1 shows the dipstick in its ‘dry’ state and an example of a positive test. Table 1.3 shows the main false negative and false positive results that can interfere with correct interpretation.
Table 1.2 The main causes of differently coloured urine
Pink–red–brown–black
Yellow–brown
Blue–green
Gross haematuria
(e.g. bladder or renal tumour; IgA nephropathy)
Jaundice
Drugs
: chloroquine, nitrofurantoin
Drugs
: triamterene
Dyes
: methylene blue
Haemoglobinuria
(e.g. drug reaction)
Myoglobinuria
(e.g. rhabdomyolysis)
Acute intermittent porphyria
Alkaptonuria
Drugs
: phenytoin, rifampicin (red); metronidazole, methyldopa (darkening on standing)
Foods
: beetroot, blackberries
Figure 1.1 Urine dipstick—the urine on the right is normal and the colours of all of the squares on the urine dipstick are normal/negative. The urine on the left is from someone with acute glomerulonephritis, looks pink-brown macroscopically and has maximal blood and protein on the dipstick.
Table 1.3 The main causes of false negative and false positive testing from use of urine dipsticks
Test
False positive
False negative
Haemoglobin
Myoglobin
Ascorbic acid
Microbial peroxidases
Delayed examination
Proteinuria
Very alkaline urine (pH 9)
Tubular proteins
Chlorhexidine
Immunoglobulin light chains
Globulins
Glucose
Oxidizing detergents
UTI
Ascorbic acid
Discounting contamination from menstrual—or other—bleeding, and exercise-induced haematuria and proteinuria.
Urine microscopy can only add useful information to urinalysis when there is a reliable methodology for collection, storage and analysis. This is often lacking, even in hospitals. Early-morning urine is best, with rapid sample centrifugation. Under ideal circumstances cells (erythrocytes, leucocytes, renal tubular cells and urinary epithelial cells), casts (cylinders of proteinaceous matrix), crystals, lipids and organisms can be reliably identified where present in urine. Figure 1.2 shows a red cell cast in urine (indicative of acute renal inflammation). Figure 1.3 shows urinary crystals.
Figure 1.2 Microscopy of centrifuged fresh urine. There is a red cell cast (protein skeleton with incorporated red blood cells). This is characteristic of acute glomerulonephritis.
Figure 1.3 Crystalluria.
Non-visible Haematuria
Definition and Background
In healthy people red blood cells (rbc) are not present in the urine in > 95% of cases. Large numbers of rbcs make the urine pink or red.
Non-visible haematuria (NVH) (formerly known as microscopic haematuria) is commonly defined as the presence of greater than two rbcs per high power field in a centrifuged urine sediment. It is seen in 3–6% of the normal population, and in 5–10% of those relatives of kidney patients who undergo screening for potential kidney donation.
NVH can be an incidental finding of no prognostic importance, or the first sign of intrinsic renal disease or urological malignancy. It always requires assessment, and most often requires referral to a kidney specialist or to a urologist.
Clinical Features
The finding of NVH is usually as a result of routine medical examination for employment, insurance or GP-registration purposes in an otherwise apparently healthy adult. Initially, therefore, NVH is an issue for primary healthcare workers. The goal of an assessment is to understand whether:
there are any clues available from the patient's history, his/her family history or from examination to point to a particular diagnosis, e.g. connective tissue disease, sickle cell disease;
the haematuria is transient or persistent;
there is any evidence of renal disease, e.g. abnormal renal function, accompanying proteinuria, raised blood pressure (BP);
the haematuria represents glomerular (i.e. from the kidney) or extra-glomerular (urological) bleeding.
Investigations
Typically, the full evaluation of NVH requires hospital-based investigations. Box 1.1 lists these in a logical order.
Urine microscopy and culture
should also be undertaken. The presence of dysmorphic red cells in the urine increases the possibility of intrinsic/parenchymal kidney disease as opposed to urological disease. This can only be ascertained in a specialist laboratory.
Renal structure
can be assessed with a renal ultrasound scan (this can show stones, cysts and tumours). A plain abdominal film will show radio-opaque renal, ureteric or bladder calculi. Renal function should be assessed by measurement of plasma biochemistry and estimated glomerular filtration rate (eGFR). In addition, proteinuria should be looked for by dipstick analysis of the urine and, if present, a protein/creatinine ratio measured. Proteinuria > 0.5 g/24 h (protein:creatinine ratio > 50) suggests glomerular disease and a referral to a kidney specialist is warranted for NVH with significant proteinuria, raised BP or abnormal renal function.
Management
Any patient who presents with persistent non-visible haematuria over the age of 40 should be referred to a urologist. A renal ultrasound, urine cytology and a flexible cystoscopy to exclude urological cancer would normally be undertaken.
Any patient who has abnormal renal function, proteinuria, hypertension and a normal cystoscopy should be referred to a kidney specialist.
Renal biopsy is required to establish a diagnosis with absolute certainty in most cases of ‘renal haematuria’. Those patients who additionally have renal impairment, heavy proteinuria, hypertension, positive autoantibodies, low complement levels or have a family history of renal disease should be considered for a renal biopsy.
Please also see the 2008 NICE CKD guidelines for further information on NVH, http://www.nice.org.uk/nicemedia/live/12069/42119/42119.pdf.
Prognosis
The prognosis for most patients with asymptomatic NVH without urological malignancy and no evidence of intrinsic renal disease is very good. It is beyond the scope of this chapter to discuss the prognosis of all the causes of non-visible haematuria, as listed in Table 1.4. However, some general observations apply for those patients in whom there is no structural cause for NVH and bleeding is glomerular, and these are given below.
Table 1.4 Causes of non-visible haematuria
Renal causes
Systemic causes
Miscellaneous and urological causes
IgA nephropathy
Systemic lupus erythematosus
Cystic diseases of the kidney
Thin basement membrane disease
Henoch–Schönlein purpura
Papillary necrosis
Alport's syndrome
Urothelial tumours
Focal segmental glomerulosclerosis
Renal and bladder stones
Membranoproliferative glomerulonephritis
Exercise-induced haematuria
Post-infectious glomerulonephritis
In the presence of impaired renal function, it is mandatory to try to achieve blood pressure control (<130/80 mmHg) and reduction of microalbuminuria or proteinuria (if present). Angiotensin converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs) are useful agents, as they achieve both of these desired effects. It is very important to recheck plasma creatinine and potassium about 7–14 days after starting ACE or ARB, and regularly thereafter—an increase of ≥ 30% in plasma creatinine or a fall of ≥ 25% eGFR, or a rise of plasma potassium to exceed 5.5 mmol/L, should occasion recall to consider abandoning the drugs or reducing the dose, further investigations, and dietary advice for potassium restriction if relevant.
It is important that these patients, whether monitored in the community or at a hospital-based clinic, have their urine tested, BP measured and renal function monitored regularly. If not under renal specialist follow-up, the development of hypertension, proteinuria or deterioration in renal function are all indications for referral to a specialist unit (see Chapter 3).
Microalbuminuria and Proteinuria
Protein is normally present in urine in small quantities. Tubular proteins (e.g. Tamm-Horsfall) and low amounts of albumin can be detected in healthy people. Microalbuminuria (MAU) refers to the presence of elevated urinary albumin concentrations (see Table 1.5); MAU is a sign of either systemic or renal malfunction.
Table 1.5 Equivalent ranges for urinary protein loss
MAU is measured by quantitative immunoassay—and is an important first and early sign of many renal conditions, particularly diabetic renal disease and other glomerulopathies. It is also strongly associated with adverse cardiovascular outcomes. Around 10% of the population can be shown to have persistent MAU. For confirmation, two out of three consecutive analyses should show MAU in the same three-month period.
UAER (urinary albumin excretion rate)—in a healthy population the normal range for UAER is 1.5–20 µg/min. UAER increases with strenuous exercise, a high-protein diet, pregnancy and urinary tract infections (UTIs). Daytime UAER is 25% higher than at night (so for daytime urine, an upper normal limit of 30 µg/min is often used). Overnight timed collections can be performed (and microalbuminuric range is an overnight UAER of 20–200 µg/min), but for unselected population screening the albumin:creatinine ratio (ACR) in early-morning urine is preferable. An ACR of > 2 predicts a UAER of > 30 µg/min with a high sensitivity.
Increasingly favoured as a screening tool is the urinary protein:creatinine ratio (PCR). This is best done on ‘spot’ early-morning urine samples (as renal protein excretion has a diurnal rhythm; see below). This is now preferable to relying on 24-hour urine collections. There is an inherent assumption in using PCR that urinary creatinine concentration is 10 mmol/L (in practice it can range from 2 to 30), but this is of little practical importance for its use as a screening tool. A PCR of 100 mg/mmol corresponds roughly to 1 g/L of proteinuria.
One question often asked is how to ‘convert’ an ACR to a PCR. At low levels of proteinuria (<1 g/day), a rough conversion is that doubling the ACR will give you the PCR. At proteinuria excretion rates of > 1 g/day, the relationship is more accurately represented by 1.3×ACR = PCR.
Table 1.5 attempts to display all of the different ways to express urinary protein to allow for comparisons between methods.
Please note that the normal range for protein excretion in pregnancy is up to 300 mg/day, with clinical significance (pre-eclampsia or renal disease) being more likely once 500 mg or more is excreted per day. See Chapter 6.
Please also see the 2008 NICE CKD guidelines on albuminuria, proteinuria and eGFR, http://www.nice.org.uk/nicemedia/live/12069/42119/42119.pdf.
Tests of Kidney Function
The kidney has exocrine and endocrine functions. The most important function to assess, however, is renal excretory capacity, which we measure as glomerular filtration rate (GFR). Each kidney has about 1 million nephrons, and the measured GFR is the composite function of all nephrons in both kidneys. Conceptually, it can be understood as the (virtual) clearance of a substance from a volume of plasma into the urine per unit of time. The substance can be endogenous (creatinine, cystatin C) or exogenous (inulin, iohexol, iothalamate, 51Cr-EDTA, 99mTc-DTPA). This ‘ideal substance’ to measure kidney function does not exist—ideal characteristics being free filtration across the glomerulus, neither reabsorption from nor excretion into renal tubules, existing in a steady state concentration in plasma, and being easily and reliably measured. Despite creatinine failing several of these criteria, it is universally used, and we shall concentrate on interpreting creatinine concentration in urine and blood as it aids derivation of GFR.
The basic anatomy of the kidney and the anatomy and basic physiology of the ‘nephron’ (the functional component of the kidney), are shown in Figure 7.1.
Table 1.6 shows the different ways in which both plasma urea and plasma creatinine may be ‘artefactually’ elevated or reduced, which can lead to misunderstanding and miscalculation of renal function. Creatinine is measured by two quite different techniques in the laboratory—one, the Jaffe reaction, relies on creatinine reacting with an alkaline picrate solution but is not specific for creatinine (e.g. cephalosporins, acetoacetate and ascorbate), while the other, the enzymatic method, is more accurate. Eventually, isotope-dilution mass spectroscopy (IDMS) may render both of these variously flawed techniques redundant, either by direct substitution of method or by allowing IDMS-traceable creatinine values to be reported.
Table 1.6 Problems with sole reliance on plasma concentrations of urea and creatinine to determine renal function
Factors independent of renal function that can affect plasma urea
Factors independent of renal function that can affect plasma creatinine
Other factors that can affect interpretation of plasma creatinine values
Hydration Burns Steroids Diuretics Liver disease Diet (protein)
Diet (meat) Creatine supplements (e.g. body builders) Age Body habitus Race
Use of Jaffe reaction in laboratories: interference by glucose, ascorbate, acetoacetate Use of enzymatic reaction in laboratories: interference by ethamsylate or flucytosine
Creatinine is produced at an almost constant rate from muscle-derived creatine and phosphocreatine. However, as can be seen from Figure 1.4, it is an insensitive marker of early loss of renal function (fall in GFR), and as renal function declines there is correspondingly more tubular creatinine secretion. It varies with diet, gender, disease state and muscle mass.
Figure 1.4 Relationship between plasma creatinine and glomerular filtration rate.
Estimated Glomerular Filtration Rate
The manipulation of plasma creatinine to derive a rapid estimation of creatinine clearance is very useful clinically, and is now formally recommended (as of April 2006—see Chapters 3 and 4) to aid appropriate identification and referral of patients with CKD. There are several formulaic ways of doing this, and the formula that has been adopted in the United Kingdom, United States and many countries is the four-variable Modification Diet in Renal Disease (MDRD) equation (Figure 1.5 and Chapter 3), but it must be appreciated that this formula has not been validated in ethnic minority patients, in older patients, in pregnant women, the malnourished, amputees or in children under 16 years of age.
Figure 1.5 Four-variable Modification Diet in Renal Disease equation for estimated glomerular filtration rate.
Useful though deriving a value for GFR is, the value derived using the MDRD formula is only an estimate whose accuracy diminishes as GFR exceeds 60 mL/min, and values should therefore be viewed as having significant error margins rather than being precise. Values can only properly be used when renal function is in ‘steady state’, i.e. not in acute kidney injury. It is unwise to rely exclusively on the formula when the eGFR is between 60 and 89 mL/min (CKD stage 2), because of its shortcomings, while values > 90 mL/min should be reported thus (i.e. not as a precise figure). There is an urgent unmet need for better markers, and better formulae.
Formal nuclear medicine or research-laboratory-derived measures of GFR are expensive, time-consuming and largely (and increasingly) confined to research studies.
Please also see the 2008 NICE CKD guidelines for the assessment and interpretation of kidney function/eGFR, http://www.nice.org.uk/nicemedia/live/12069/42119/42119.pdf.
Renal Imaging
There is a wide range of imaging techniques available to localize and interrogate the kidneys. Table 1.7 gives the preferred methods for a range of conditions. Intravascular contrast studies are still used, though ultrasound has replaced most IVU/IVP (Intravenous urogram/intravenous pyelogram) examinations. Low osmolar non-ionic agents are less nephrotoxic and better tolerated. Reactions to contrast agents can be severe, though rarely life-threatening. In addition, renal impairment (usually mild and reversible, sometimes severe and irreversible) can be seen after the use of intravenous contrast. In patients with a plasma creatinine > 130 µmol/L (eGFR <60 mL/min), thought must be given to the wisdom of the investigation. Pre-existing renal impairment, advanced age, diabetes and diuretic use or dehydration significantly increase the risk of contrast-induced nephropathy. The mainstay of prevention is understanding the risk and avoiding dehydration (by judiciously hydrating patients and promoting urine flow) using saline or 0.45% sodium bicarbonate. The dopamine agonist fenoldopam and the antioxidant N-acetylcysteine have both been proposed as protective agents; oral N-acetylcysteine has been widely assessed with conflicting results and its role remains uncertain. However, it is an inexpensive agent without significant side-effects, and its use in clinical practice may not therefore be inappropriate.
Table 1.7 Renal imaging techniques and their main indications/applications
Condition
Technique
Renal failure
Ultrasound
Proteinuria/nephrotic syndrome
Ultrasound
Renal artery stenosis
MRA
Renal stones
Plain abdominal film
Non-contrast CT
Renal infection
Ultrasound or CT abdomen
Retroperitoneal fibrosis
CT abdomen
MRA, magnetic resonance angiogram.
A comprehensive review of all imaging techniques is beyond the scope of this chapter. We shall concentrate on ultrasound imaging as this is by far the most often used for screening and investigation. Reference to radionuclide imaging and IVU/IVP is made in Chapter 12. Renal size is usually in proportion to body height, and normally lies between 9 and 12 cm. Box 1.2 shows reasons for enlarged or shrunken kidneys. The echo-consistency of the renal cortex is reduced compared to medulla and the collecting system. In adults the loss of this ‘corticomedullary differentiation’ is a sensitive but non-specific marker of CKD. Apart from renal size and corticomedullary differentiation, the other significant abnormalities reported by ultrasound include the presence of cysts (simple, complex), solid lesions and urinary obstruction. Figure 1.6 shows a normal kidney (a) and an obstructed kidney (b). Examination of the bladder and prostate is usually undertaken alongside scanning of native (or transplanted) kidneys.
Figure 1.6(a) Ultrasound appearance of a normal kidney: dark areas represent renal cortex, and the central white area is the renal pelvis and collecting system. (b) An obstructed kidney, which shows in its centre a severely dilated renal pelvis and calyces (containing urine which is ‘dark’ on ultrasound).
Renal angiography and other techniques relevant to renal blood vessels are covered in Chapter 8. Radionuclide imaging is used for renal scars and urinary reflux, which is also mentioned in part in Chapter 12.
Renal Biopsy
A renal biopsy is undertaken to investigate and diagnose renal disease in native and transplanted kidneys. Table 1.8 shows the main indications, contra-indications and complications of this test. It is a highly specialized investigation, which should only be performed after careful consideration of the risk/benefit ratio, and with the close support of experienced imaging and renal histopathological teams.
Table 1.8 Indications for renal biopsy
Indications
Contraindications
Complications
Nephrotic syndrome
Multiple renal cysts
Pain
Systemic disease with proteinuria or kidney failure
Solitary kidney (relative)
Bleeding—haematoma, haematuria (significant in <5%)
Acute kidney injury
Acute pyelonephritis/abscess
Other organ biopsied (e.g. colon, spleen, liver)
Proteinuria (PCR > 50–100)
Renal neoplasm
Arteriovenous fistula (0.1%)
Proteinuria and micro/macro-haematuria
Uncontrolled blood pressure
Nephrectomy (<0.1%)
Unexplained chronic kidney disease
Abnormal blood clotting
Death (<0.01%)
Transplanted kidney
Morbid obesity (relative)
Inability to consent to, or to comply with instructions
PCR: protein:creatinine ratio.
Further Reading
Fink HA, Ishani A, Taylor BC, Greer NL, MacDonald R, Rossini D, Sadiq S, Lankireddy S, Kane RL, Wilt TJ (2012) Screening for, monitoring, and treatment of chronic kidney disease stages 1 to 3: a systematic review for the U.S. Preventive Services Task Force and for an American College of Physicians Clinical Practice Guideline. Ann Intern Med 156(8):570–81.
Maione A, Navaneethan SD, Graziano G, Mitchell R, Johnson D, Mann JF, Gao P, Craig JC, Tognoni G, Perkovic V, Nicolucci A, De Cosmo S, Sasso A, Lamacchia O, Cignarelli M, Manfreda VM, Gentile G, Strippoli GF (2011) Angiotensin-converting enzyme inhibitors, angiotensin receptor blockers and combined therapy in patients with micro- and macroalbuminuria and other cardiovascular risk factors: a systematic review of randomized controlled trials. Nephrol Dial Transplant 26(9):2827–47.
NHS Evidence: http://www.evidence.nhs.uk/topic/kidney-failure
Redon J, Martinez F (2012) Microalbuminuria as surrogate endpoint in therapeutic trials. Curr Hypertens Rep 14(4):345–9.
Van de Wal RM, Voors AA, Gansevoort RT (2006) Urinary albumin excretion and the renin-angiotensin system in cardiovascular risk management. Expert Opin Pharmacother 7(18): 2505–20.
www.renal.org/eGFR/haematuria.html
www.renal.org/eGFR/proteinuria.html
www.renal.org/eGFR/refer.html
http://www.nice.org.uk/nicemedia/live/12069/42119/42119.pdf
