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THE KIDNEY AND URETER (DUPLEX SYSTEM (instead of a single metanephric mass…

- - - - excess of normal constituents
        
        inc concentration of solutes in the urine, because of either a low urine volume or increased excretion, may result in precipitation from a supersaturated solution
        
        inc excretion of calcium (hypercalciuria) may be secondary to hypercalcaemia or more commonly idiopathic
        common causes of an inc in serum calcium are hyperparathyroidism and prolonged immobilisation (Eg a paraplegic person confined to bed)
        
        inc serum uric acid may be accompanied by uric acid stone formation. the most common cause is gout but it may also occur following chemotherapy for leukaemia, lymphoma or polycythaemia
        
        inadequate urine volume: renal stones are particularly common in people from temperate climates who go to live in the tropics, where dehydration produces extremely concentrated urine
        
        inc oxalate excretion results from increased dietary intake, with strawberries, rhubarb, leafy vegetables and tea having high levels of oxalate.
        hyperoxaluria is also a complication of loss of their terminal ileum (eg in Crohn's disease or after surgical resection), which results in increased oxalate absorption by the colon.
      - lack of inhibitors of stone formation
        
        low levels of citrate and magnesium in the urine make calcium complexes less soluble, which promotes calcium oxalate and phosphate stone formation
      - inadequate drainage
        
        calculi may form whenever urine flow is poor, eg within a hydronephrosis or in a diverticulum of the bladder
      - presence of abnormal constituents
        
        foreign bodies such as non absorbable sutures inserted at op, ureteric stents, sloughed necrotic renal papilla or a fragment of broken urinary catheter, may act as a nidus for stone formation
        
        vitamin a deficiency which may occur in primitive communities, results in hyperkeratosis of the urinary epithelium, which again provides the debris upon which stones may form
        
        urinary infection - particularly in the presence of obstruction eg hydronephrosis or chronic retention, produces epithelial cell sloughing and this may act as a nidus for stone formation.
        in addition, infection may alter the urine pH, favouring precipitation of certain solutes. a high pH, brought about by the presence of urea-splitting organisms such as Proteus, favours calcium phosphate stone formation for example.
        
        cystinuria caused by a mutation in one of two different genes responsible for amino acid transfer in the kidney, may result in cystine stone formation
  - - - phosphate stones (33%) are composed of a mixture of calcium,ammonium and magnesium phosphate (triple phosphate stone) they are hard, white and chalky. they are nearly always found in an infected urine and produce the large staghorn calculus deposited within a pyonephrosis
      - oxalate stones (calcium oxalate) are the most common (60%). they are hard with a sharp, spiky surface, which traumatises the urinary tract epithelium; this causes bleeding that usually colours the stone a dark brown or black
      - uric acid and urate stones (5%) are moderately hard and brown in colour with a smooth surface. Pure uric acid stones are radiolucent but, fortunately for diagnosis, most contain enough calcium to render them opaque to X-rays
      - cystine stones account for about 1% of urinary calculi
      - note that a stone found in the lower urinary tract may have arisen there primarily or it may have migrated there from a primary source within the kidney
  - - - IX of underlying cause
        
        analysis of the stone should be performed
        
        uric acid esimation: the serum uric acid is raised in gout with its associated uric acid is raised in gout with its associated uric acid stones
        
        urine microscopy and culture: the urine is cultured for bacteria and examined microscopically for the presence of cystine crystals
        
        serum calcium estimation is carried out - ~1% of stone formers have hypercalcaemia, occasionally due to a parathyroid adenoma
      - diagnostic ix
        
        CT is the investigation of choice to determine whether pain is due to a urinary tract stone or other pathologies (eg torted ovarian cyst, ruptured aortic aneurysm) and to confirm the size and site of the stone
        
        plain abdo x-ray specifically looking at kidneys, ureters and bladder (KUB) will show the presence of stone in 90% of cases
        
        MAG3 renography (mercapto-acetyl triglycine) may also be used to determine the presence of obstruction and impairment of function
        
        urine is tested for the presence of blood
  - - - analgesia, ideally an NSAID to relieve severe pain. the great majority of small stones within the ureter (up to 5mm) pass spontaneously. these ureteric stones tend to lodge at one of 3 places
        
        point at which ureter crosses pelvic brim
        
        entrance of ureter into the bladder (vesicoureteric junction)
        
        PUJ
      - the lower the sstone, the more likely it is to pass spontaneously
        stone passage is promoted by tamsulosin - alpha blocker - medical expulsive therapy
    - - if the stone remains in the ureter following an epsiode of acute colic and cannot or will not pass despite medical expulsive therapy, intervention is necessary to avoid renal impairment due obstruction
        extra-corporeal shock wave lithotripsy (ESWL) is first line
        other options:uteroscopywith some disintegration by holium laser, electrohydraulic lithotripter, or extraction with the aid of a Dornia basket
    - - a small calculus lodged in the solid substance of the kidney without symptoms can be left alone but kept under periodic survey
        larger renal stones require removal
        initially ESWL may be removed percutaneously using a nephroscope (percutaneous nephrolithotomy)
        small symptomatic lower pole stones, which tend to be difficult to target with ESWL, may be treated by flexible uteroscopy and laser ablation
    - - this may be due to blockage of both ureters by stones or obstruction of a solitary kidney
        it is best treated by percutaneous nephrostomy, although retrograde ureteric stenting is an alternative.
        temporary renal replacement therapy (haemofiltration) may also be required. the stone is then removed as indicated above
- - - - haematuria
      - loin pain, usually aching
      - abdo mass - asymptomatic, bilateral, lobulated renal swellings found on routine examination
      - UTI
      - renal failure presenting with headache, lassitude, vomiting and refractory anaemia
      - HTN
      - intracranial haemorrhage, as a result of HTN or berry aneurysm
    - - Classical signs of uremia are: progressive weakness and easy fatigue, loss of appetite due to nausea and vomiting, muscle atrophy, tremors, abnormal mental function, frequent shallow respiration and metabolic acidosis.
- - - - 1) hydronephrosis secondary to obstruction:
        a) within the lumen, eg ureteric calculus
        b) in the wall eg urothelial carcinoma, congenital pelviureteric junction obstruction owing to neuromuscular inco-ordination
        c) outside the wall eg retroperitoneal fibrosis, extrinsic tumour such as cervical cancer
      - 2) Hydronephrosis without obstruction: vesicoureteric reflex
- - - - when normal flap valve mechanism at the vesicoureteric junction is deficient, urine can pass back up the ureter during bladder contraction
        this flap valve failure can occur as an isolated finding or with an ectopic ureter in a duplex system
    - - the collecting ducts enter the calyx of the renal pelvis on a renal papilla - 2 types
        
        compound papillae common in polar region of kidney, the ducts open perpendicular to surface of calyx and dont close as intrarenal press rises; intrarenal reflux occurs
        
        simple (convex) papillae - ducts open at oblique angle = press within calyx inc, ducts close, preventing urine from refluxing into kidney (intrarenal reflux)
      - if urine is infected the resulting inflam leaves a permanent scar and loss of nephrons.
        neighbouring papillae are distorted by scarring allowing further intrarenal reflux = repeated episodes of infection = major damage and loss of function
- - - - RENAL
        
        include factors directly acting upon the glomerular apparatus and tubules
        
        myoglobin secondary to rhabdomyolysis eg following a crush injury or reperfusion of an ischaemic limb
        
        drugs eg abx eg gentamicin or NSAID eg diclofenac
        
        Acute cortical necrosis, due to severe ischaemia
        
        acute nephritis - interstitial nephritis or glomerulonephritis
        
        acute tubular necrosis (ATN)
      - POSTRENAL (obstructive)
      - PRE-RENAL
        
        fluid loss
        
        blood loss eg haemorrhage
        
        plasma loss eg burns, generalised peritonitis
        
        electrolyte loss eg vomiting, diarrhoea, fistula, inadequate replacement
        
        impaired circulation
        
        general factors eg hypotension due to sepsis, cardiac failure
        
        local factors eg aortic dissection in which the renal arteries are excluded from the circulation
        
        regulatory mechanisms maintain renal perfusio - GFR normally maintained even if the mean arterial pressure falls to 60-80mmHg
        in hypertensive pts, elderly or pre-existing renal disease (g diabetic nephropathy - autoreg may be impaired and GFR maintained only at higher mean pressures
        NSAID and ACEi can impair compensatory mechanisms
  - - - best signs
        
        JVP not visible
        
        postural hypotension
      - treatment requires rapid infusion of a fluid that remains in the intravasc compartment = blood, colloid, salinr but not dextrose
        infusion continued until JVP is visible and postural hypotension corrected
        K+ additives not given until diuresis is established since patients are likel to be hyperkalaemic
      - central venous catheter to measure CVP IF SEPTIC OR CARDIAC DISEASE may want pulm art catheter - capillary wedge pressure and to determine systemic vasc resistance = indicate requirement of inotropes
      - infusion stopped once vol repletion achieved and stopped until urine output picks up to prevent overload
    - - if rehydration unsuccessful in inducing a diuresis, a bolus of furosemide should be given a low dose dopamine infusion has beenused in this setting but recent evidence questions its efficacy
      - if these measures fail to induce diuresis it is likely that either ATN or less commonly acute cortical necrosis has occurred
    - - K+ >6.5 treat it immediately! to avoid ventricular arrhythmias - ECG = tented t waves, p waves disappear, ecg becomes sinusoidal or may even have no ECG changes
      - calcium gluconate given over few mins to stabilise myocardium
        insulin and dextrose infused over 10-20min = drive k+ into cells
        for longer fix need diuresis if flop then dialysis
        potassium exchange resins eg calcium resonium oral or enema may give good interim potassium control - however cause constipation so need laxative - lactulose twice daily
- - - - most commonly incidental finding on imaging
      - triad of symptoms of a renal cell carcinoma present in well <10% of cases
        
        loin pain aching in 40%
        
        loin mass presenting in 25%
        
        haematuria in half of cases - may produce clot colic
      - rarely a left varicocele may occur (1%) as a consequence of tumour spread
    - - may present with the general features of malignancy - anaemia, loss of weight and occasionally a pyrexia of unknown origin or as a consequence of mets eg a pathological fracture
    - - a no. of hormones may be released from renal cell carcinoma. clinical consequences may be HTN (renin production), polycythaemia (erythropoietin) andhypercalcaemia (ectopic parathormone production)
        O/E diseased kidney may be palpable
- - - - severe HTN persisting after renal injury
      - lack of function in the affected kidney after several mths but only if symptomatic (eg recurrrent infections, stone formation)
      - continued bleeding, which threatens life
- - - - Women with recurrent = ix, in men/child with one infection is unusual so investigate
        
        US of bladder and kidneys may demonstrate a large residual vol of urine within the bladder or hydronephrosis
        
        plain abdo x-ray - to exclude a bladder stone as a source of recurrent infection
        
        urine microscopy and culture - usually E Coli. the presence of pus cells with no growth of bacteria on culture (Sterile pyuria) is most often due to incompletely treated infection, but can be seen in bladder cancer and TB of urinary tract
        
        cystoscopy may be necessary to exclude bladder cancer, stone or bladder diverticula
- - - - stone
      - ulcerating TB
      - tear
      - tumour
      - parenchymal disease eg nephritis
      - cystitis
      - distended veins over large prostate
    - - urethra - trauma, stone and cancer
      - ureter - cancer and stone
      - kidney - cancer, stone, infection, glomerulonephritis, trauma, polycystic disease, TB and infarction eg from emboli in infective endocarditis
      - bladder - infection (cystitis), cancer, stone, trauma and bilharzia
      - prostate - BPH, cancer
  - - - Haematuria accompanied by pain in one or the other loin suggests renal origin, and intermittent pain indicates a stone in the renal pelvis or ureter or partial ureteric obstruction by clot or necrotic papilla
      - terminal bleeding with severe pain and frequency indicates a bladder cause, usually infection
        prostatic bleeding is more likely to be initial or terminal and usually painless
      - dribbling of blood from the urethra independent of micturition is typical of a urethral origin for the blood
      - completely painless and otherwise symptomless haematuria is suggestive of a tumour in the urinary tract
      - a hx of recent sore throat esp in a child would make a diagnosis of acute nephritis a possibility
        always check whether the pt is on anticoag therapy or if there is a hx of bleeding tendencies; haematuria while on anticoag is still more commonly due to renal tract patholgoy which the anticoag has made symptomatic - full ix is warranted
    - - one or other kidney may be palpable. an enlarged prostate, particularly if the pt is hypertensive may suggest a prostatic source of bleeding, although other causes must be excluded before this diagnosis is made
    - - urine cytology - look for evidence of malignancy; cytology is best at detecting high-grade tumours
      - US - detect parenchymal tumours, renal calculi and lesions in the collecting system and bladder
      - urine microscopy - the presence of red cells will exclude haemoglobinuria and beeturia (following beetroot)
        the presence of casts will indicate nephritis; pus cells and organisms suggest infection
      - contrqast enhance CT - principal imaging modality for ix of visible haematuria
      - cystoscopy - will show any intravesical lesion in addition to bleeding from the prostate or blood emerging from one or the other ureter
        flexible cystoscopy may be performed under local anaesthetic at the initial clinic visit
- - - - benign
        
        oncocytoma (uncommon tumour, characteristic 'scar' on CT)
        
        ANGIOMYOLIPOMA (UNCOMMON HAMARTOMA, CHARACTERISTIC ct APPEARANCE)
        
        adenoma (small and symptomless)
        
        Haemangioma (A rare cause of haematuria
      - malignant
        
        primary - nephroblastoma, renal cell carcinoma
        
        secondary - the kidney is an uncommon site for deposits of carcinomaalthough it may be involved in advanced cases of lymphoma and leukaemia as well as tumours of breast and bronchus
    - - urothelial carcinoma
      - squamous carcinoma
      - papilloma
      - 2 principal malignant tumours of the kidney are nephroblastoma in children and renal cell carcinoma in adults