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The urinary tract comprises the kidneys, pelvicalyceal systems, ureters, bladder and urethra. The kidney is responsible for excretion of the waste products of metabolism, the waste products being excreted in the form of an aqueous solution called urine . Urine passes from the kidneys into the pelvicalyceal systems and thence via the ureters to the bladder, which acts as a reservoir. Urine is held in the bladder by a series of muscular sphincters until sufficient volume has accumulated. Relaxation of the sphincters and contraction of smooth muscle in the bladder wall allows the urine to be voided to the exterior through the urethra (micturition) at a convenient time.
The kidney is divided into two main anatomical divisions, the cortex and medulla ( E-Fig. 15.1 H ). Disorders of the kidney may affect either of these zones, but diseases affecting one part will often have secondary effects on the other component. Disorders may arise from a wide range of pathological causes, many of which are common in other organ systems (e.g. infections, tumours, drug reactions, vascular disorders). However, the kidney is unusual in that it is much more prone to immunological disorders than most other organs. Vascular diseases such as hypertension, diabetes mellitus and vasculitis may also have profound effects on renal function. Disorders of the kidney can be conveniently divided into categories according to which structural component of the kidney is primarily affected:
Glomerulonephritis (GN ) of various types, most of which are due to deposition of immunoglobulins and/or complement components (collectively called immune complexes ) within the glomerulus ( Figs 15.2 to 15.7 ).
Vasculitis: strictly speaking, this is a vascular disorder, but some forms affect the glomerular capillaries giving the clinical and pathological appearances of a GN. ( Fig. 15.3 )
Ischaemia: common systemic diseases, including hypertension and diabetes mellitus, as well as a range of thrombotic and embolic conditions may cause glomerular injury.
Disorders involving deposition of material in the glomerulus
Diabetes mellitus: deposition of abnormal glycosylated proteins causes irreversible structural and functional abnormalities in the glomerulus ( Fig. 15.9 ).
Amyloidosis: deposition of amyloid proteins in the glomerulus alters the structure and therefore the function of the glomerulus ( Fig. 15.10 ).
Congenital and structural abnormalities: some inherited conditions result in abnormal glomerular structure and function; an example is the condition thin basement membrane disease.
Acute tubular necrosis (ATN) is usually due to profound hypotension causing ischaemic damage to tubular epithelial cells. Some forms of drug toxicity may give rise to similar appearances.
Interstitial nephritis (AIN) is an important cause of acute renal failure and is most often due to drug hypersensitivity.
Infections including acute and chronic pyelonephritis , renal abscess and TB.
Mechanical obstruction of the ureters or bladder may lead to hydronephrosis and recurrent infection.
Hypertension causes marked changes to both large and small renal vessels. The changes of benign/essential hypertension and accelerated/malignant hypertension are discussed in Fig. 15.15 .
Thrombotic microangiopathy is a pattern of vascular damage that results in intravascular thrombosis due to endothelial cell injury. It is typically seen in association with haemolytic anaemia, thrombocytopenic purpura and often renal failure. Although many of the pathological changes are due to damage to the microcirculation, especially the glomerular capillaries, thrombosis also occurs in larger vessels.
Vasculitis may affect larger vessels as well as glomerular capillaries, but the main manifestations are usually glomerular.
Diabetes mellitus is an important metabolic disease that has profound vascular effects, affecting both large vessels and the microvasculature.
Damage to one component of the kidney inevitably damages the other parts. Severe reversible damage to any of the above components of the kidney may lead to acute renal failure or acute kidney injury (AKI) . Some conditions are reversible, e.g. some types of AKI and most cases of acute diffuse proliferative GN, but many lead to progressive damage. In cases with progressive damage, there will be some degree of permanent renal impairment and a proportion of these will develop chronic renal failure , a condition that was invariably fatal until the advent of renal dialysis and kidney transplantation.
Acute renal failure: Abrupt cessation of activity of the nephrons usually presents initially as a marked fall in urine production (oliguria) , which may even be total (anuria) . This is accompanied by a rapid rise in serum urea and creatinine levels. Disturbances of fluid and electrolyte balance soon follow, particularly a rise in the serum potassium level and metabolic acidosis.
Chronic renal failure : Progressive retention of nitrogenous metabolites causes a slow rise in serum creatinine levels due to insufficient glomerular filtration. Concomitant failure of tubular function produces widespread abnormalities in biochemical homeostasis, including salt and water retention, metabolic acidosis and other electrolyte imbalances, particularly hyperkalaemia.
F fibrosis of glomerulus In interstitial space P protein cast T tubule
Glomerular disorders arise from a variety of causes; the two major causes being immunological (including disorders confined to the kidney and some systemic diseases) and metabolic (the most important being diabetes mellitus). It is confusing to many students that there is not a direct one-to-one relationship between a particular mechanism of damage and a particular histological appearance and/or clinical syndrome. In fact, most causes of glomerular damage will give rise to one of several clinical presentations, summarised in Table 15.1 , along with the diseases with which they are most commonly associated. Acute and chronic renal failure are described above and may supervene in any of the above conditions. For example, an individual with a severe nephritic syndrome may progress quickly to acute renal failure or an individual with undiagnosed diabetes mellitus, who has had undetected proteinuria for some time, may first be diagnosed with chronic renal failure.
The introduction of safe and reliable techniques of percutaneous needle biopsy of the kidney has greatly increased knowledge about the natural history of renal diseases, particularly by elucidating the underlying lesion early in the course of glomerular diseases when treatment might be applied effectively. It is of limited value in chronic renal failure when the kidney is shrunken and histological changes are non-specific, i.e. end-stage kidney ( Fig. 15.1 ). Renal biopsy is also frequently used in the assessment of renal transplants to detect the presence of transplant rejection, drug toxicity and a number of other conditions that may cause reduced function of the graft. Maximum information is obtained from a needle biopsy of renal tissue using a combination of the following methods:
Light microscopy , including special stains to define glomerular structures
Electron microscopy to show the presence and precise location of immune complexes, which appear as irregular deposits of electron-dense material (dense deposits) , and other deposits such as amyloid, diabetic changes, structural changes to the glomerular basement membrane (GBM) and podocytes.
Immunofluorescence microscopy to localise and identify the class of immunoglobulins and complement components.
|Syndrome||Clinical features||Histological changes||Associated disease|
|Acute nephritis|| Haematuria, Hypertension, Uraemia (↑BUN)
Oedema (often periorbital), Oliguria or anuria
|Hypercellular glomerulus with obstructed capillary loops|| Acute post-infective GN
IgA nephropathy/Henoch-Schönlein purpura
|Nephrotic syndrome||Proteinuria (3.5 g/24 h), Hypoalbuminaemia, Oedema, Hyperlipidaemia||Changes to the structure of the glomerular filtration mechanism, including the GBM and/or podocytes|| Diabetes mellitusAmyloidosis
Minimal change nephropathy
Focal segmental glomerulosclerosis
|Mixed nephritic– nephrotic syndrome||Features of both nephritic and nephrotic syndromes||Both cellular proliferation and GBM alterations|| Membranoproliferative GN (mesangiocapillary GN)
|Asymptomatic haematuria||Periodic dark-coloured urine or microscopic haematuria||Proliferation of glomerular cells or structural abnormalities of GBM|| IgA nephropathy
Thin basement membrane disease
|Asymptomatic proteinuria||Proteinuria||Early stages of the changes in the GBM seen in the nephrotic syndrome||Early phases of all of the conditions which cause nephrotic syndrome|
The immunofluorescence and electron microscopic patterns of immune complex deposition can be vital to differentiate between different types of GN, which have similar patterns of glomerular damage by light microscopy. Examples include:
IgA nephropathy: granular deposits of IgA in the mesangium
Membranous nephropathy: granular deposits of IgG and complement on the epithelial side of the GBM
Goodpasture’s syndrome: linear deposits of IgG along the GBM
Systemic lupus erythematosus (SLE): deposits of most classes of immunoglobulin and many complement components at any site in the glomerulus
Interpretation of a renal biopsy also requires information about the clinical history, physical examination and other investigations to arrive at a correct diagnosis. For example, a membranous pattern of GN might be idiopathic, related to use of certain drugs (e.g. gold, penicillamine) or may be part of the spectrum of SLE (Class V lupus nephritis).
Most types of GN are caused by immune complex deposition in the glomerulus. This applies to primary GN , where the condition is confined to the kidney (e.g. membranous nephropathy , membranoproliferative GN ), and to diseases with a systemic component (e.g. Goodpasture’s syndrome , SLE , Henoch-Schönlein purpura ).
The site of immune complex deposition is dependent on the size of the complexes, which is in turn dependent on the type of antigen and on the class of immunoglobulin produced, i.e. the host response. The antigen may be either a normal component of the body (a self antigen as in Goodpasture’s) or an external antigen such as a bacterial product (as in post-streptococcal GN ). Immune complexes may be deposited from the circulating blood or may be formed in situ. In the latter situation, the complexes may involve intrinsic glomerular antigens (basement membrane components in Goodpasture’s) or antigens that have been deposited there from the circulation (e.g. DNA in the case of SLE). An important exception to this rule is minimal change nephropathy where the podocytes are thought to be damaged by a cell-mediated immune response, rather than by immune complex deposition.
Whatever the mechanism of damage to the glomerulus, the various immunological insults alter the structure and therefore the function of the glomerulus and ultimately of the nephron as a whole.
In response to damaging stimuli, the glomerulus appears to react in one or more of the following ways:
Swelling and/or proliferation of the normally flat endothelial cells lining the glomerular capillaries
Proliferation of the epithelial cells investing the outer surface of the glomerular capillary tuft (the podocytes ( E-Fig. 15.4 H ) and the cells lining Bowman’s capsule (crescent formation)
Thickening of glomerular basement membranes ( E-Fig. 15.5 H )
Proliferation of the cells of the mesangium and excessive production of acellular mesangial material
These reactions give rise to various histological patterns of GN, which can be identified by light microscopy. This is then put together with the immunofluorescence and electron microscopy findings, clinical history and other investigations to come to a definitive diagnosis. As in many other areas of histopathology, good communication between pathologists and clinicians is vital to arrive at an accurate diagnosis, which is essential for appropriate treatment.
Patterns of GN may be described as:
Diffuse: affecting all glomeruli
Focal: affecting some glomeruli
Global: the entire glomerulus is abnormal
Segmental: only part of the glomerulus is abnormal
We shall now consider some specific examples of GN, reviewing the typical histological and immunofluorescence patterns and their associated clinical presentations. As indicated in Table 15.1 , some diseases may present clinically in several different ways, with nephritic or nephritic features or even combinations of these.
For convenience, we shall begin with disorders which typically give rise to acute nephritic features ( acute diffuse proliferative GN ; Fig. 15.2 and necrotising GN ; Fig. 15.3 ) followed by those with mixed patterns of haematuria and proteinuria ( mesangial proliferative GN ; Fig. 15.4 and membranoproliferative GN ; Fig. 15.5 ) and then important causes of nephrotic syndrome ( membranous GN ; Fig. 15.6 , focal segmental glomerulosclerosis ; Fig. 15.7 and minimal change disease ; Fig. 15.8 ).
At the end of this section on glomerular diseases, we shall consider the typical changes of diabetes mellitus in the kidney ( Fig. 15.9 ) and the features of renal amyloidosis ( Fig. 15.10 ). It is worth bearing in mind that primary GN is a relatively rare disease, whilst diabetes and hypertension together account for the bulk of clinically important renal dysfunction in developed counties; in the developing world, toxins and infections are also very important factors in the burden of chronic renal disease.
N neutrophils U urinary space
B normal glomerular basement membrane C crescent D double contour basement membrane F fibrin M increased mesangial matrix and cellularity N normal glomerular segment R glomerular remnant
This new classification affecting MPGN is based upon immunofluorescence findings. If immunoglobulins are identified as well as C3, the disease is viewed as immunoglobulin-mediated and is still defined as MPGN type I or type III, depending upon the location of the immune complexes. In contrast, those cases with isolated C3 in the glomerulus fall within the category of C3 nephropathy . Morphological and EM patterns vary and almost any pattern of glomerular damage can occur in C3GN, although MPGN is most common. All cases formerly called MPGN type II or dense deposit disease are now known to fall within this spectrum, as do a proportion of those previously classified as types I or III (now called C3 glomerulonephritis or C3GN ).
We now know that these patients have various congenital or acquired abnormalities affecting the alternative pathway of complement activation, some of which can be detected by serological tests or by genetic screening. Testing should be offered whenever the renal biopsy findings are of glomerulonephritis with dominant C3. Traditionally, renal outcomes in patients with MPGN were quite varied and some groups, including those with dense deposit disease, had a high chance of recurrence in transplanted kidneys. As well as conventional immunosuppressant drugs, there are now emerging targeted therapies such as anti-C5 antibodies, which may modify the underlying disease process in some patients.
B glomerular basement membrane DD dense deposit M mesangial matrix S spike Sc sclerosis
The renal disorders in which the major abnormality involves the glomerulus may subside spontaneously or with treatment. However, if they progress, glomerular blood flow is obstructed, glomerular filtration ceases and the tubules associated with affected glomeruli become involved; thus many nephrons may cease to function. When sufficient nephrons have been affected, the clinical features of the disease gradually progress to chronic renal failure.
By way of illustration, a patient with the nephrotic syndrome caused by diabetic glomerular disease may slowly develop the features of chronic renal failure as individual nephrons are destroyed. In contrast, a patient who initially presents with the acute nephritic syndrome caused by a rapidly progressive GN with extensive crescents ( Fig. 15.3 ) may quickly progress to acute renal failure. As the glomeruli are rapidly destroyed by the disease process this becomes irreversible.
BM glomerular basement membrane C capsular drop En endothelial cell cytoplasm FC fibrin cap H hyalinised arteriole K Kimmelsteil-Wilson nodule P podocyte foot process
The tubules and interstitium may be primarily damaged as a result of hypovolaemic shock, by inorganic and organic toxins or as the result of infection. In hypovolaemic states and intoxication, tubular epithelial cells may exhibit marked cytoplasmic degenerative changes or frank necrosis leading to the pathological term acute tubular necrosis ( Fig. 15.12 ) and producing the clinical syndrome of acute renal failure. Tubular epithelial cells have considerable powers of recovery and regeneration and acute renal failure may be reversible under such circumstances if the patient can be sustained in the interim by dialysis and other supportive measures.
Another increasingly important cause of tubulo-interstitial disease is drug toxicity giving rise to interstitial nephritis ( Fig. 15.13 ). In this condition, a large number of drugs have been implicated including certain antibiotics, non-steroidal anti-inflammatory drugs, thiazide diuretics and proton pump inhibitors. Onset may be acute or chronic. There is a mixed inflammatory infiltrate in the interstitium in which eosinophils may be prominent. Tubular damage occurs and the condition may proceed to chronic renal failure.
Infections of the kidney include acute and chronic pyelonephritis and tuberculosis (see Ch. 5 ). Acute suppurative bacterial infections of the kidney ( pyelonephritis ) usually follow ascending infection from the lower urinary tract, particularly when there is obstruction to urinary outflow such as in benign prostatic hyperplasia or pressure from the fetus in pregnancy; in such cases, coliform organisms (such as Escherichia coli and Proteus species) are the most frequent infecting agents. Infection may also spread to the kidney by the haematogenous route during episodes of bacteraemia. Acute pyelonephritis may be complicated by the development of papillary necrosis ( Fig. 15.14 ) or pus accumulation in a dilated, obstructed pelvicalyceal system ( pyonephrosis ) . Acute pyelonephritis is illustrated in Fig. 15.11 . Tuberculous infection of the kidneys and lower urinary tract may also arise by similar routes of spread.
Patients with urinary reflux or obstruction are prone to develop recurrent pyelonephritis Repeated attacks lead to scarring and after many episodes the kidney becomes coarsely scarred, a phenomenon termed chronic pyelonephritis .
AA afferent arteriole G glomerulus N neutrophil polymorphs T dilated tubule
The kidney is especially vulnerable to the effects of arterial hypertension as illustrated in Figs 11.1 and 11.2 , and irreversible damage to nephrons may result either acutely from accelerated (malignant) hypertension or progressively over a period of years in benign (essential) hypertension.
Hypertensive nephrosclerosis resulting from benign (essential) hypertension is illustrated in Fig. 15.15 . Malignant or accelerated hypertension causes a different pattern of renal damage, similar to the changes seen in acute scleroderma , and may result in acute renal failure. In reality, hypertension cannot be neatly divided into essential and accelerated types; individuals who have had mild hypertension for many years may progress quite suddenly to very high blood pressures that put eyesight, kidneys and other organs at severe risk. This is especially the case where the individual has underlying renal disease that progresses. Other individuals may develop accelerated hypertension out of the blue.
Various forms of vasculitis may also affect the kidney, including polyarteritis nodosa (see Fig. 11.6 ) and those associated with antineutrophil cytoplasmic antibody (ANCA) such as granulomatosis with polyangiitis (previously known as Wegener’s granulomatosis) and microscopic polyarteritis (see Fig.11.7 ).
Small infarcts of the renal cortex are common in patients with the above vascular disorders. They are usually seen as incidental findings in kidneys removed for other reasons (e.g. tumours). The infarcts are usually seen as wedge-shaped pale scars with the base abutting the renal capsule, although they may be seen in any stage of infarction (see Fig. 10.1 ). In kidneys with extensive infarcts, the cortical surface is pitted and the kidney is shrunken. In rare cases, abrupt interruption to the blood supply, such as renal artery thrombosis, may lead to renal cortical infarction where the entire renal cortex undergoes coagulative necrosis. The renal medulla is much more resistant to ischaemia.
D dilated tubules E eosinophil I mononuclear inflammatory cells J junction between normal and necrotic tissue O interstitial oedema P renal papilla T tubulitis
AA afferent arteriole H hyalinised sclerosed glomerulus S segment of glomerulus
Renal transplantation has become a routine treatment for chronic renal failure in many countries. The transplant recipient is freed from a life of regular dialysis with a consequent improvement in quality of life. The function of the transplanted kidney may however be affected by a number of factors in the days, weeks and months following transplantation. The most important of these include:
Acute tubular necrosis : this is identical to acute tubular necrosis from other causes ( Fig. 15.12 ). The major factor here is the ‘cold ischaemic time’, i.e. the length of time between harvesting of the kidney and re-establishment of vascular perfusion in the donor. Supportive measures may be needed in the immediate post-transplantation phase but usually this will resolve.
Rejection (see Fig. 15.16 )
Drug toxicity : routinely used immunosuppressive agents, such as ciclosporin A and related compounds (the calcineurin inhibitors), may have a range of effects on the kidney. Histologically, there may be changes in the tubules and/or the blood vessels. Exquisite control of dosage and sometimes transfer to a different agent will usually control this problem.
Infection : transplant recipients require immunosuppression to prevent rejection of the graft and this makes them susceptible to a range of infections.
Recurrent GN : this is more likely to be a problem months to years after transplantation than in the early stages.
A adipose tissue I intimal arteritis M smooth muscle cells N tumour cell nest S oedematous stroma SM smooth muscle of artery wall T tubulitis V blood vessels
A range of benign and malignant tumours occurs in the kidney and many are unique to the kidney. Benign tumours include papillary adenoma , a fairly common incidental finding in nephrectomy specimens, oncocytoma , illustrated in Fig. 15.17 , and angiomyolipoma , shown in Fig. 15.18 .
The most common and important malignant renal tumour in adults is renal cell carcinoma. Several subtypes are recognised and some of the more common variants are illustrated in Fig. 15.19 . One of its important methods of spread is by venous invasion, typically giving rise to ‘cannon ball’ lung metastases and often bone metastases.
Our understanding of renal tumour pathology has been transformed in recent years by the use of new molecular techniques. Classification is now based upon a combination of histological appearances, immunohistochemical findings and the presence of typical genetic changes in certain tumour types. For example, papillary renal cell carcinomas typically show gains of chromosomes 7 and/or 17, as well as loss of the Y chromosome. These new investigative techniques have also revealed a range of rare but important hereditary renal cell carcinomas.
The kidney is the site of an important malignant tumour of children, nephroblastoma or Wilms’ tumour ( Fig. 15.20 ); this is an example of a ‘small round blue cell tumour’ and is of embryological origin.
C undifferentiated cells G normal glomeruli I inflammation M foamy macrophages P papillary structures T malignant tubules Tu primitive tubular structures V blood vessel
The most important disorders of the lower urinary tract are infection and neoplasia. Infections are common, but usually remain confined to the bladder (cystitis) ; ascending spread into the ureters and pelvicalyceal systems may result in renal parenchymal involvement (acute pyelonephritis) as shown in Fig. 15.11 . Persistent or repeated infection in the urinary tract predisposes to the development of urinary stones (calculi) , particularly in the bladder and pelvicalyceal systems. Infections of the urethra (urethritis) are commonly sexually transmitted, often involving the organisms N. gonorrhoeae and Chlamydia .
The pelvicalyceal system, ureters and bladder are lined by a specialised epithelium known as transitional epithelium (urothelium) ( E-Fig. 15.11 H ). Malignant tumours of the urothelium, known as transitional cell or urothelial carcinomas ( Fig. 15.22 ), are common and are of particular interest because of the possible role of chemical carcinogens such as aniline dyes in their pathogenesis. Urothelial carcinomas may be either invasive or non-invasive. Most of the deeply invasive tumours are high-grade carcinomas. Malignant tumours are probably preceded by the development of urothelial dysplasia and carcinoma in situ ( Fig. 15.21 ). Benign tumours include transitional cell papillomas and inverted papillomas .
Classification and grading of transitional cell neoplasms is complex and continues to evolve. The traditional WHO 1973 system recognised benign papillomas as well as transitional cell carcinomas of grades 1, 2 and 3. This system has some limitations as the criteria for these categories are not very well defined and a large proportion of tumours tend to be classified as grade 2. Also, some tumours that are now known to behave in a benign fashion are classified as grade 1 carcinomas. The newer WHO/ISUP 2004 system uses the term papillary urothelial neoplasm of low malignant potential (PUNLMP) for these very low grade tumours with likely benign behaviour and it splits the remaining malignant tumours into low grade and high grade groups. The two systems do not directly correspond. Despite the limitations described above, the old 1973 WHO classification remains in widespread use as a validated and reproducible system, but now it is used alongside the newer WHO/ISUP 2004 system as these are thought to provide the best prognostic information when applied in conjunction. This is illustrated in Table 15.2 .
BV blood vessels M mitotic figures S stroma SM smooth muscle T tumour
|WHO 1973 classification||WHO/ISUP 2004 classification|
|Transitional cell carcinoma Grade 1||Papillary urothelial neoplasm of low malignant potential (PUNLMP)|
|Transitional cell carcinoma Grade 2||Low-grade urothelial carcinoma|
|Transitional cell carcinoma Grade 3||High-grade urothelial carcinoma|
|Site||Disorder||Main pathological features||Figure|
|Kidney: glomerular disorders||End-stage kidney||Sclerosed glomeruli, atrophic tubules, interstitial fibrosis||15.1|
|Acute diffuse proliferative GN||Enlarged hypercellular glomeruli, infiltration by neutrophils, obstructed capillary loops||15.2|
|Necrotising GN||Necrosis of glomerular tuft, may be segmental, may be associated with crescent formation||15.3|
|Mesangial proliferative GN||Expanded mesangium with increased mesangial cells||15.4|
|Membranoproliferative (mesangiocapillary) GN||Hypercellular, hyperlobular glomeruli with double contour GBM||15.5|
|Membranous nephropathy||Thickened GBM, ‘spikes’ (silver stain)||15.6|
|Focal segmental glomerulosclerosis||Idiopathic or secondary to segmental necrosis or nephron loss. Segment of tuft replaced by fibrosis||15.7|
|Minimal change disease||Normal light microscopy and immunofluorescence, ‘fused’ podocyte foot processes on electron microscopy||15.8|
|Diabetic nephropathy||Diffuse and nodular glomerulosclerosis, hyalinised arterioles, capsular drops, fibrin caps, thickened GBM||15.9|
|Renal amyloidosis||Deposition of insoluble fibrillar protein in glomerulus and vessel walls, stains with Congo and Sirius red||15.10|
|Kidney: interstitial disorders||Acute pyelonephritis||Infiltration of interstitium and tubules by neutrophil polymorphs. May form abscesses and pyonephrosis||15.11|
|Acute tubular necrosis||Dilated renal tubules with flattened ‘simplified’ epithelium, vacuolation and fragmentation of tubular cell cytoplasm||15.12|
|Acute tubulo-interstitial nephritis||Often due to drug hypersensitivity. Interstitial oedema with eosinophils and mononuclear cells. Focal tubulitis||15.13|
|Renal papillary necrosis||Infarction of renal papilla with inflammation at edge of infarcted area||15.14|
|Kidney: vascular disorders||Essential hypertension||Hypertrophied arteries with fibroelastic intimal thickening, sclerosed glomeruli||15.15A|
|Accelerated hypertension||Fibrinoid necrosis of arterioles, ‘onion-skin’ intimal thickening of medium and large sized arteries, vascular thrombosis, acute ischaemia of glomeruli||15.15B|
|Kidney: transplant rejection||Acute T-cell mediated rejection|| Inflammation of tubules (tubulitis) and interstitium (type I)
Inflammation of arteries (intimal arteritis, transmural arteritis, fibrinoid necrosis of artery wall (types II and III))
|Kidney: tumours||Oncocytoma||Brown tumour macroscopically, often with central scar. Nests of bland epithelial cells with round nuclei and eosinophilic granular cytoplasm||15.17|
|Angiomyolipoma||Mixture of abnormal blood vessels, smooth muscle cells and adipose tissue. Most are benign||15.18|
|Renal cell carcinoma|| Clear cell: cells have clear cytoplasm
Papillary: papillary epithelial structures with foamy macrophages in papillary cores
Chromophobe: cells with pale-stained cytoplasm and prominent cell borders
Collecting duct: infiltrating tumour with desmoplasia
|Nephroblastoma||Primitive undifferentiated cells, tubular structures||15.20|
|Bladder||Carcinoma in situ||Flat lesion consisting of highly atypical epithelial cells with mitotic figures and no maturation of cells towards the surface||15.21|
|Urothelial carcinoma (transitional cell carcinoma||Papillary structures covered by abnormal urothelial cells. High grade lesions may form solid ulcerated plaque. Graded as high or low (and/or 1, 2, 3)||15.22|