Urology Flashcards
What are the normal levels of water consumption and urine production for dogs and cats?
Dog 50-100ml/kg/day water, cats 30-50/ml/kg/day
Urine production dogs <50ml/kg/day (1-2ml/kg/hr)
Cat - 25-50ml/kg/day (1-2ml/kg/hr).
What is the function of the kidney?
Control of fluid balance (renal concentrating ability), control of acid base ( hydrogen ion excretion, bicarbonate regeneration), excretion of electrolytes (sodium, potassium calcium, phosphate), excretion of waste products (urea, creatinine, toxic metabolites, drugs). Filtration and reabsorption (glucose, proteins). Endocrine functions (erythropoietin, calcitriol).
What is anuria?
Absence/negligible production of urine by the kidneys.
What is azotaemia?
Increased levels of nitrogenous waste products (urea and creatinine) within the blood
What is oliguria?
Decreased production of urine by the kidneys. (0.25-1.9ml/kg/hr)
What is periuria?
Urination in an Inappropriate place (typically cats out with litter box) unlike incontinence (involuntary passage of urine), these patients usually have control over their urination i.e behavioural)
What is pollakiuria?
Frequent passage of small volumes of urine
What is stranguria??
a passage of a narrowed stream of urine.
What is uraemia?
clinical signs associated with loss of adequate percentage of functional nephrons. typical signs may include halitosis (uraemic breath), anorexia (gastritis), vomiting (gastritis and effect on cTZ), neurological signs, muscle weakness.
Why is it important to get an accurate history i.e how can this affect your diagnosis?
Incontinence may be present continuously only when asleep only on exitement (urge incontinence) or may occur at the end of urination. if blood is present the timing of this may help to localise the source. blood at the start of urinaration may reflect urethral vaginal, penile or preputial disease, whereas blood at th end may reflect renal, ureteric or bladder disease. blood throughout the stream may be present with upper or lower urinary tract disorders. dogs with prostatic disease may drip blood independent of urination. it is important to remember that haematuria may also be associated with non urogenital conditions such as coagulopathies.
What might you find on physical exam of the urinary tract?
The kidneys should be evaluated for size, margination and pain, the bladder should be palpated gently - size assessed and the presence/absence of pain. if the bladder feels hard this may suggest bladder wall thickening and cystic calculi may be appreciated as hard masses within the bladder. a rectal exam should be performed to evaluate the urethra in female and male dogs, the prostate in male dogs.
What properties are evaluated in urinalysis?
Urine concentrating ability which reflects tubular function (urine specific gravity). loss of concentrating ability develops when approximately 2/3 of the nephrons are damaged resulting in a low USD. biochemical properties e.g glucose, ketones, bilirubin. presence of protein in the urine (proteinuria), which reflects glomerular function. this is quantified further by the urine protein:creatinine ratio. sediment analysis, bacterial culture.
How does biochemistry appear with urinary tract disease?
Routine biochemistry may be normal especially with lower urinary tract disease. with renal disease, evaluations in urea, creatinine and phosphorus may be seen, as the kidney loses its ability to excrete these substances. it is also important to measure electrolytes, as potassium and calcium may be increased or decreased. ideally ionised calcium should be measured rather than total calcium. Measurement of protein levels is important as albumin may become low with glomerular disease.
What may haematology identify in urinary tract disease?
Haematology may identify increased PCV in patients that are dehydrated or reduced PCV in patients with anaemia. the latter may be associated either with blood loss from the urogenital tract or chronic kidney disease. Increased white blood cell counts may be seen with infectious disease processes. abnormally shaped red blood cells (poikillocytes) may also be seen with marked azotaemia.
What is azotaemia?
Urea and creatinine are the nitrogenous waste products typically elevated in azotaemia. urea is produced by the liver from ammonia, and creatinine is released from muslce. urea levels can be affected by dietary protein (increased) and liver function ( decreased). Creatinine levels can be affected by muscle mass, emaciated animals may have a normal creatinine in the presence of renal disease. unfortunately elevate urea and creatinine levels on blood profile are often assumed to indicate kidney disease but this is not always the case.
What is pre renal azotaemia?
azotaemia develops as a result of reduced renal perfusion, which lowers glomerular filtration rate. reduced perfusion may occur as a result of reduced blood flow for a number of reasons such as hypovolaemia, hypotension, poor cardiac output, or constriction of the afferent arteriole. Urea may be disproportionately higher than creatinine although this may also reflect a high protein meal. urine specific gravity is often high normal in cases of pre renal azotaemia, particularly those associated with dehydration. Pre renal azotaemia is usually reversible by addressing the underlying problem
What is renal (intrinsic) azotaemia?
Azotaemia develops as a result of damage to the nephron, preventing adequate glomerular filtration. Approximately 75% of functional nephrons have to be damaged before a patient will develop azotaemia, therefore absence if azotaemia does not necessarily reflect normal renal function. renal Azotaemia is accompanied by the presence of inadequate renal concentrating ability, reflected in a low urine specific gravity. the USG may be thee same osmolality as plasma i.e isothenuric.
What is post renal azotaemia?
Azotaemia develops as a result of inability to eliminate urine produced by the kidneys. this may be due to rupture or obstruction of the urinary tract. rupture of a rueter, the bladder or urethra leads to urine in the abdomen. urea and potassium are absorbed across the peritoneum, with creatinine following more slowly. obstruction can lead to distension of the ureter and or kidney (hydroureter and hydronephrosis) causing decreased glomerular filtration as a result of increased pressure in bowmans space. as with pre renal azotaemia, renal function is often restored if the underlying problem is addressed.
Describe what may be seen on diagnostic imaging of the urinary tract?
Plan radiographs allow evaluation of renal size, number and margination. mineralisation may be appreciated, particularly radio opaque nephroliths and cystic calculi. size and location of bladder may also be evaluated. ultrasonography allows a better assessment of renal parenchyma. fine mineralisation and cystic lesions within the kidneys may be identified. ureters may be identified, particularly if distended. the bladder wall can be more fully assessed and non radio opaque cystic calculi and blood clots can be identified. contrast radiography - both poitive and negative contrast studies can be performed including intravenous urography to assess kidneys and ureters, pneumocystogram to assess size and location of bladder, as well as bladder wall thickening, double contrast cystography to assess for bladder wall thickening and intra luminal structures such as calculi or clots and retrograde urethrography. Computed tomography - may allow more accurate assessment of renal structure and location of ectopic ureters. cystoscopy - allow assessment of urethral, ureteric openings and intra luminal structure within the bladder, it an also facilitate non invasive biopsy sampling of the bladder.
How is glomerular filtration rate assessed?
The gold standard to assess renal function is measurement of the glomerular filtration rrate. this typically involves measurement of clearance of an inert substance that is freely filtered by the glomerulus, without reabsorption or secretion in the tubules. inulin, endogenous creatinine and exogenous creatinine have been used. Exogenous creatinine is difficult to source and laboratory measurement of inulin is not readily available. radio isotopes and scintigraphy have also been used.
When is renal biopsy indicated?
This may be indicated for glomerular disease, where specific diagnosis may result in improved treatment. consideration has to be given to risks, namely anaesthesia in Azotaemic patients, how the biopsy will be obtained (surgical vs percutaneous ultrasound guided tru-cut) and complications (haemorrhage, worsening azotaemia) versus benefit obtained. an alternative may be cytology from fine needle aspirates, particularly if renal lymphoma is considered likely.
What are renal biomarers?
Retinol binding protein, N -acetyl-B-D -glucosaminidase (NAG), cystatin C and urinary yGT potentially may be able to detect renal tubular damage at an earlier stage before azotaemia develops.
What is the difference between renal insufficiency and renal failure?
Renal insufficiency is often used to describe reduced function of the kidneys (manifest by proteinuria or loss of tubular concentrating ability and low specific gravity and occurs with approximately 66% nephron loss.) Renal failure is used to describe reduced glomerular filtration rate resulting in azotaemia and subsequently uraemia and occurs with approximately 75% nephron loss.
What is renal dysplasia?
A congenital condition resulting in disorganised development of renal parenchyma, it requires histopathology to confirm the presence of immature glomeruli but is often suspected based on abnormal ultrasonographic appearance of kidneys in a young dog. a number of breeds are affected including boxers, chows, golden retrievers, lhasa apsos, shih tzus and miniature schnauzers.
What is unilateral renal agenesis?
Absence of one kidney, may occasionally be identified. the remaining kidney is often hypertrophied to compensate and affected animals may be asymptomatic.
What is polycystic kidney disease?
A familial condition primarily affecting persian cats, but may also affect BSH cats, bull terriers, WHWT and cairn terriers. anechoic cysts may be detected by ultrasonography and genetic testing is also available for persian cats. Other familial renal diseases include basement membrane disorders, glomerulonephritis, amyloidosis and tubular disorders such as Fanconi’s syndrome.
What are renal infections/pyelonephritis?
The upper urinary tract is usually a sterile environemtn. infection may establish in the kidneys from haematogenous spread, but more typically occursa as a result of loss of innate defence mechanisms allwing ascending infection from the bladder. the concentrated nature of urine and ureteric peristalsis normally protects against infeciton. dilute urine, glucosuria and trauma damaging the urothelium may allow establishment of infection as well as obstructive disorders and vesico ureteric reflux. pyelonephritis is renal inflammation.
What are the signs of an acute renal infection?
PU/PD, haematuria, lethargy, vomiting, anorexia, renal pain, pyrexia. renal pan may be difficult to localise from abdominal pain and may also be confused with lumbar pain. chronic conditions may be less apparent although PUPD is usually present and there may be ahistory of recurrent lower urinary tract infections. Urinalysis may reveal dilute urine with active sediment (casts, white blood cells, red blood cells.) culture is required to identify causal orgnaism. Azotaemia may or may not be present. Good empiric choice of amoxicillin-clavulanate - bactericidal, concentrates in urine, broad spectrum. Extended course typically 4-6 weeks often prescribed.
What is the primary role of the glomerulus
Filtration of the plasma through a permselective membrane the BM that filters or retains substances based on their size and charge. damage to the glomerulus leads to loss of the selectivity of the BM and filtration of substances, predominantly proteins, into the urine that are not normally present. glomerular diseases may be generally classified into glomerulonephritis and amyloidosis but they are both characterised by significant proteinuria often with uPC in excess of 10. Persistent proteinuria can lead to tubular damage with the development of azotaemia.
What is glomerulonephritis?
different forms of glomerulonephritis exist however electron microscopy of a renal biopsy is required to differentiate them. immune complexes and infectious agents can play an important role in damaging the BM, and familial disease may result in abnormal BM formation.
What is amyloidosis?
Amyloid is a protein that is formed from serum amyloid A (an acute phase protein). its deposition within the kidney may be associated with chronic inflammatory diseases, although there are familial tendencies in sharpei dogs and abysinnian, siamese and oriental cats. In cats, the amyloid tends to be deposited within the medulla, so the degree of proteinuria may not be so extensive. Specific diagnosis of these conditions requires a renal biopsy although significant proteinuria, particularly if accompanied by hypoalbuminaemia will raise the suspicion for glomerulonephritis or amyloidosis. management is non specific and aimed at removing any underlying infectious or inflammatory causes. addressing the proteinuria with ace inhibitors and supplying a good quality diet with w33 supplementation, aspirin may be used to reduce the risk of thrombo embolic disease.
What are the renal tubules responsible for?
They are responsible for reabsorption of glucose, electrolytes and small amounts of protein filtered by the glomerulus. control of acid base status and water balance also occurs in the tubules. the most common tubular disorders are acute kidney injury and chronic kidney disease, but primary tubular disorders can also occur.
What is fanconi syndrome?
This may be congenital, with the basenji being the most commonly affected breed. it may also be acquired for example with infections such as leptospirosis. renal tubular reabsorption is affected, resulting in loss of variable amounts of glucose, amino acids, bicarbonate and electrolytes in the urine. fanconi syndrome may be suspected in a polyuric, polydipsia patient with Glucosuria but not hyperglycaemia. further assessment may include measuring urinary electrolytes and amino acids. treatment is primarily supportive e.g nutrition and bicarbonate supplementation, the condition will invariably progress to CKD.
What is primary renal glucosuria?
This may be a congenital defect (norweigan elkhounds, scottish terriers) or acquired secondary to tubular damage. diagnosis is based on identifying persistent glucosuria in the absence of hyperglycaemia or loss of other substances in the urine. Management is primarily aimed at controlling urinary trat infections to which these cases are prone and ensuring adequate caloric intake.
What is renal tubular acidosis?
These disorders result in a metabolic acidosis and may be congenital or acquired. proximal renal tubular acidosis arises when the proximal tubules cannot reabsorb bicarbonate ions and is often part of fanconis syndrome. This usually results in mild acidaemia due to compensatory acid secretion by the distal renal tubules and urine with a pH of 5.5-6.0. Distal renal tubular acidosis arises when the distal tubules cannot secrete hydrogen ions. As this is more significant factor in acid base homeostasis the metabolic acidosis arising is usually marked and the urine pH>6.0. Management o these conditions include identifying and addressing underlying causes and alkalinisation therapy typically with potassium citrate.
What is diabetes insipidus?
diabetes insipidus arise due to lack of anti diuretic hormone (central) or insensitivity of the kidney to effect of anti diuretic hormone (nephrogenic diabetes insipidus) this reuslts in inability to concentrate the urine with production of large volumes of dilute urine and compensatory polydipsia. most forms of NDI are acquired e.g due to hyperadrenocorticism, chronic kidney disease, liver disease, pyometra, pyelonephritis, hyperthyroidism or drugs 9corticosteroids, diuretics).
What is acute kidney injury?
Acute kidney injury reflects a sudden reduction in renal function. Often difficult to identify a specific cause. the kidneys are at particular risk for ischaemia as although they only comprise 0.5% of body weight, they receive 20% of cardiac output. the renal cortex receives 90% of renal blood flow and it sustains the majority of the damage due to its high metabolic demands and concentration of nephrotoxins in the tubular epithelial cells. Ischaemia and toxic damage results in tubular cell apoptosis and necrosis. damage to the renal tubule may also invoke an inflammatory response which can lead to further ischaemia as capillaries become plugged with platelets and neutrophils.
What are the 4 phases of acute kidney injury?
Initiation: the patient has been exposed to the caudal agent, but clinical signs may not be present. intervention at this stage may prevent progression. Extension: inflammation and hypoxia lead to further nephron damage which can be fatal if the damage is too extensive. maintenance: irreversible damage has occurred and the patient has on going signs of reduced tubular function. Recovery: regeneration and repair of the damaged nephrons may occur over a period of weeks to months.
Describe the common causes of AKI in veterinary patients?
Ischaemia - anaesthesia, hypotension, hyperviscosity
Infarction - thrombi and emboli eg cardiac disease, neoplasia
Toxins - ethylene glycol, lilies, grapes, raisins, heavy metals, organic compounds, haemoglobin, myoglobin, envenomation, melamine. Infectious diseases - leptospirosis, pyelonephritis, borrelia burgdorferi (lymes diseasE), feline infectious peritonitis. Drugs - NSAIDS, aminoglycosides, amphotericin B, cisplatin, radiographic contrast agents, sulphonamides, tetracyclines, ACE inhibitors. Hypercalcaemia - rodenticides, psoriasis creams , neoplasia. Severe illness- SIRS, sepsis, acute pancreatitis, pyometra, multiple organ dysfunction syndrome, disseminated intravascular coagulation DIC, heat stroke, immune mediated haemolytic anaemia.
What are the clinical signs of AKI?
Patients with AKI will typically have short <1week history of signs such as anorexia, nasea, lethargy, vomiting, diarrhoea, weakness, and possibly altered mentation. Polyuria and polydipsia are not always present if the patient is anuric/ooliguric. Physical examination will usually reveal patients in good bodily cndition. the degree of dehydration may be variable, depending on e.g frequency of vomiting. A uraemic breath and or oral ulceration may be detected. Renal palpation may reveal painful + enlarged kidneys. The bladder may be detected. Renal palpation may reveal painful, enlarged kidneys. The bladder may be enlarged or non palpable if the patient is dehydrated or anuric. If mucous membranes are icteric then this may raise the suspicion for leptospirosis and barrier nursing should be employed. if bradycardia is identified this should raise the suspicion that hyperkalaemia may be present.
What Investigation should be done for AKI?
Routine haematology - may be normal or reveal an inflammatory leucogram if infectious disease is present. anaemia is generally more suggestive of chronic kidney disease, but could occur with AKI. Routine biochem - azotaemia, phosphorous likely to be elevated, calcium concurrently elevated - suspicion of vitamin D toxicity and increases the risk of ongoing damage from nephrocalcinosis. potassium may be elevated as a result of reduced renal tubular excretion. Acid base status - patients with AKI are frequently acidotic due to inability to excrete hydrogen ions and synthesis bicarbonate. Urinalysis : USG is typically low. gluosuria in the absence of hyperglycaemia is supportive of renal tubular damage. Imaging: ultrasonography generally more helpful to evaluate renal parenchyma than radiography, although renal enlargement and mineralisation may be detected. abnormalities seen with AKI may include hyperechoic cortices ethylene glycol renal pelvic proximal ureteric dilation, nephrolithiasis or uterolithiasis and hydronephrosis.
What are the differential diagnosis which must be ruled out with AKI?
CKD, post renal azotaemia, pre renal azotaemia and hypoadrenocorticism. It is generally not possible to distinguish AKI fomr CKD based on laboratory parameters alone. patients with CKD typically have an insidious onset of signs, are in poorer body condition, may be anaemic and are likely to have small kidneys rather than large kidneys. patients with CKD may decompensate suddenly if for example they become dehydrated or get an infection (so-called acute on chronic disease). hypoadrenocorticism is an important differential diagnosis as it generally requires a favourable prognosis.
What are the aims of treatment of AKI?
Ensure appropriate hydration with isotonic crystalloid (usually hartmanns or 0.9% NaCL.) Convert anuric/oliguric renal failure to polyuria to diurese uraemic toxins. address electrolyte imbalances. address acid base imbalances. provide specific therapy for the underlying disease. provide symptomatic therapy for nausea. provide nutritional support. Fluid therapy to correct dehydration and replace on going fluid deficits. fluid requirements for patients with polyuric renal failure can be substantial but if patients are anuric care must be taken that they do not become fluid overloaded. the patient should be rehydrated then if no urine is produced a fluid challenge with 5ml/kg can be given to account for sub clinical dehydration. Hyperkalaemia can be an emergency due to effect on cardiac musculature. Calcium gluconate may be given to stabilise the cardiac membrane whilst therapies to lower potassium take effect. fluid therapy will dilute the potassium and insulin and dextrose saline can be used to stimulate intracellular shift of potassium. sodium bicarbonate can also be given to encourage this.
What other treatment options are available for AKI?
Severe hypocalcaemia may be seen with ethylene glycol toxicity. administration of calcium may be necessary to address hypocalcaemic tetany and seizures. specific therapy may be difficult to provide if the underlying aetiology is unknown. where an infectious agent or sepsis is identified then appropriate intravenous antibiotics should be administered. withdrawal of potentially nephrotoxic drugs is also essential. surgery may be required if AKI is due to obstructive disorders. Supportive therapy comprises anti emetics such as maropitant and metoclopramide and gastro protectants such as H2 blockers and sucralfate for uraemic gastritis that can deelop. bathing oral mucous membranes with oral hygiene solutions may also be beneficial. if hypertension - use of amlopidine. nutritional support important to enable repair of damaged nephrons. Appetite stimulants are generally ineffective. water soluble vitamin supplementation in IV fluids may be beneficial.
What is the prognosis with AKI?
Prognosis is often poor, although outcomes are generally dependent on the underlying cause. leptospirosis and NSAID toxicity for example generally have a good outcome. for ethylene glycol particularly if anuric, outcomes are poor. Even where haemodilalysis is available, this is usually performed primarily to stabilise the patient before renal transplantation.
What is chronic kidney disease?
The loss of kidney function (dilute urine + proteinuria + azotaemia) over 3 months. althogh CKD m ay be progressive from juvenile nephropathies or as a cosequence of disease causing aki, many cases have chronic tubulo interstitial nephritis of unknown aetiology. identifying a specific aetiology may be easier in the earlier stages as progressive disease results in fibrosis, atrophy, mineralisation and inflammation, regardless of the initial cause. CKD is approximately twice as common in cats and dogs with an estimated 15-20% of cats > 15 years old.
What are the clinical signs of CKD?
Polyuria/polydisia: as the renal tubules lose concentrating ability, dilute urine is produced in alrger volumes, stimulating increased thirst to prevent dehydration. This may be harder to appreciate in cats than in dogs who often present for incontinence if they are urinating in the house overnight. hyporexia/anorexia is a decreasing appetite may be due to nausea associated with increased urea levels and gastritis associated with uraemia. vomiting may be an extension of the anorexia. weight loss is non specific and secondary to decreased appetite and also loss of protein in the urine. hind limb weakness - more apparent in cats, and can be due to both loss of muscle mass, anaemia and or hypokalaemia. a plantigrade stance can also be bserved. constipation can occur in cats, secondary to dehydration. blindness can be acute in onset due to retinal haemorrhages from hypertension. behavioural changes - often ascribed to the patient getting older and can include inappropriate vocalisation , loss of toilet training, appearing wandered, uraemic or hypertensive encephalopathy. Diagnosis may be made following investigation of a history of polyuria/polydipsia or randomly following screening blood tests or urinalysis. in advanced cases patients are generally lean or poor body condition with poor muscle mass. assessing hydration may be difficult in elderly thin animals with loss of skin elasticity. The finding of a heart murmur or gallop rhythm may indicate hypertension. cats may exhibit plantigrade stance and inability to retract the claws. retinal examination may reveal choroidal oedema, tortuous retinal vessels, retinal haemorrhages or hyphahemia. Halitosis, oral ulceration and a uraemic smell can be identified on breath as condition advances.
How do you investigate CKD?
Initial investigation will typically comprise urinalysis to confirm the presence of dilute urine. urine culture is also recommended due to the increased risk of uriinary tract infections, particularly if active sediment or bacteria are identified on sediment analysis. A UPC should also be performed to assess for proteinura. blood pressure measurement should ideally be performed prior to blood sampling, particularly if there is suspicion from the physical examination that the patient may be hypertensive. routine biochemistry will confirm the presence of azotaemia. Particular note should also be made of calcium and phosphorous levels and electrolytes. routine haematology is useful to assess if anaemia is present.
At what stage of hypertension is there risk of target end organ damage?
180mmHG - high
When is urine classified as proteinuric?
Cats – >0.4urine protein: creatinine ratio
Dogs– > 0.5
What are the ddx for CKD?
Diabetes mellitus, hyperadrenocorticism, hypercalcaemia, pyometra,hepatic disease, hyperthyroidism, medications, diabetes insipidus, psychogenic polydipsia.
How can dietary management be used to slow progression of CKD?
Protein restriction: this should not be excessive. low normal protein levels may be adequate for other than the most uraemic patients. protein restriction is often required in order to limit phosphate levels. phosphate restriction: probably the most beneficial component to dietary management. increased fat: supplies calories. Alkalinisation: patients with CKD may suffer metabolic acidosis, therefore an alkalinising agent such as potassium citrate or sodium bicarbonate may be added. Fatty acids: in dogs, alteration of the w3 to w6 ratio has been shown to be beneficial as w3 contains some anti inflammatory properties. this has not been demonstrated in cats, possibly due to differences in metabolism of fatty acids. Antioxidants: oxidant damage to protein, lipids, DNa may play a role in progression of CKD. supplementation of antioxidans such as vitamin E, carotenoids or flavanoids may prove beneficial but at present no studies have been carried out to support or refute this idea. sodium restriction is not generally advocated as there is little evidence it contributes to hypertension. restriction of sodium may infact contribute to deleterious activation of renin angiotensin aldosterone system (RAAS). Patients may be hyperkalaemic or hypokalaemic. normal potassium levels are Therefore usually fed with potassium supplementation for those that require it. Use of renal diet is advocated from IRIS stage II onwards. Inadequate nutrition will lead to catabolism of muscle tissues which will worsen azotaemia, therefore if caloric intake cannot be met with renal diet it is better to allow the animal to eat what it wants.
What is hyperphosphataemia?
The control of phosphate is important due to its contribution to ongoing renal damage and the development of secondary renal hyperparathyroidism. phosphate restriction should be initiated in patients with IRIS stage II renal disease, even if the phosphate level is within reference range. different target levels have been proposed based on classification. Initially introducing of a phosphate restriction diet should be used, with phosphate levels checked 4 weeks after starting the diet. if phosphate levels are still too high then a phosphate binder should eb introduced again and phosphate levels reassessed after 4 weeks. phosphate binders act primarily within the GI tract to reduce absorption of phosphate. options available include : aluminium salts, calcium salts, sevelamer hydrohloride, lanthanum carbonate. At present there is no studies to which is the best. calcium salts are considered less efficacious than aluminum, but a veterinary product is available. care should be taken in patients that have ionised hypercalcaemia. lanthanum carbonate has good phosphate binding ability and its veterinary formulation facilitates administration. The addition of vitamin E to the formulation provides an excellent antioxidant source.
What is proteinuria - how is it managed in renal disease?
the presence of proteinuria has been significantly associated with shorter survival times. proteinuria may be reduced by the use of an ACE inhibitor which will cause: dilation of the efferent renal arteriole, this reduces glomerular hypertension, reduction of angiotensin II, t his has an effect on systemic hypertension, may reduce podocyte hypertrophy and may reduce renal fibrosis, reduction of aldosterone, may reduce renal firosis, may increase appetite and feeling of well being, may cause an increase in azotaemia as a result of reduction in GFR, proteinuria has been shown to be deleterious and associated with a poorer outcome as it may exacerbate tubulo interstitial damage.
How is anaemia managed in cKD?
Anaemia associated with CKD is considered multi factorial in origin. contributing factors include: decreased erythropoeitin production ybt he failing kidneys, increased blood loss from GI bleeding, decreased life expectancy of circulating red blood cells, suppression of the bone marrow by uraemic toxins such as PTH, decreased precursor availability e.g iron, protein from anorexia. due to problems associated with management of anaemia, treatment should only be carried out when the patient becomes symptomatic from the anaemia. Options for treatment include erythropoeitin (eprex), darbopoeitin (aranesp) and blood transfusion.
How is uraemia managed?
Dehydration may hasten the progression of underlying renal disease. whist most patients will become polydipsic, their fluid intake may not match their urine output. ensuring adequate water is available and encouraging water consumption e.g provision of running water, flavouring of water may be beneficial. management of uraemia : use of antiemetics may contribute to restoration of appetite, although metabolism of metoclopramide may be reduced in patients with renal disease. metoclopramide is more efficient given as a constant rate infusion. uraemic gastritis can contribute to nausea and vomiting. H2 blockers and sucralphate can be used to reduce this and consideration may be given to appetite stimulants such as cyproheptadine or mirtazepine.
