Chronic Kidney Disease Flashcards
How should CKD be diagnosed?
Over a long time - at least 1m, possibly 3
Creatinine in a fasted patient at least 12 hours at least a month apart
BP readings
Proetinuria on at least 2-3 readings
Imaging studies
What are the recommendations for feeding a kidney diet?
dogs with IRIS CKD Stages 3 and 4 and cats with IRIS CKD Stages 2–4
how are kidney diets different to normal diets?
reduced protein, phosphorus, and sodium content, increased B‐vitamin and soluble fiber content, increased caloric density, a neutral effect on acid‐base balance, supplementation of omega‐3‐polyunsaturated fatty acids and the addition of antioxidants. Feline kidney diets are supplemented with potassium.
What drugs can be used to stimulate appetite?
antiemetic drugs (eg, maropitant, ondansetron), H2‐receptor blockers or hydrogen pump antagonists (eg, famotidine, ranitidine, omeprazole), and appetite stimulants (eg, mirtazapine, cyproheptadine) Consider feeding tube if cannot get BCS to near 5
How can the signs of uraemia be managed?
Management of anorexia, nausea and vomiting typically includes:
(1) limiting gastric acidity using H2 blockers,
(2) suppressing nausea and vomiting using antiemetics,
(3) providing mucosal protection using sucralfate.
Of these treatments, H2 blockers are most commonly employed and few adverse effects have been attributed to their use. The most commonly used H2 blockers include famotidine and ranitidine. However, since their efficacy remains unproven, there is only weak evidence to support a recommendation to use them
Outline the use of SC fluids
Only patients that show clinically apparent benefits to chronic fluid therapy should receive chronic supplementation with subcutaneous fluids.
Administer balanced fluid e.g. Hartmanns every 1-3 days
75-150ml per cat
Why avoid hyperphosphataemia?
hyper phosphataemia can promote renal secondary hyperparathyroidism, mineralization of tissues and progression of CKD
Do for stages 2-4
Each IRIS stage has its own upper limit of phosphate recommendation. Often this is lower than lab level
How should you manage phosphate levels
Start with kidney diet
After 6 weeks rc phosphate. If not within the ideal range then add a phosphate binder (normally an aluminum salt)
Start at low end of dose and measure/ change to effect every 4-6 weeks
How do you manage acidosis (mostly only in pets with uraemia - 50%)
Ensure renal diet
Consider use of alkanising agent ini within 4 weeks
Sodium bicarbonate or potassium citrate
Only weak evidence for use of these
It is not fully known why cats becomen hypokalaemic - many stage 2 and 3 are, very few in stage 4 are.
What are the suggested reasons for this?
inadequate potassium intake, increased urinary loss, and enhanced activation of the renin‐angiotensin‐aldosterone system due to dietary salt restriction may play a role. In addition, amlodipine may promote hypokalemia in some cats with CKD
In stage for GFR may be so low as to promote retention
How do you treat hypokalaemia?
Potassium gluconate or potassium citrate ideally oral
Measure every 7-14 days and assess need for dose change
How can anaemia be managed?
Darbopoeitin - long acting erythropoietin. Has an induction phase and a maintenance phase
Give if PCV < 20%
Check iron concentrations prior to use
Typically see an increase in PCV in 2-3 weeks
Consider a one off injection of iron at the first one. Can rarely get anaphylactic shock with this so monitor closely after
PCV should be measured weekly during the induction phase (to avoid overdosage), every other week during transition to the maintenance phase, and monthly once a stable PCV in the target range has been achieved in the maintenance phase.
Dogs may require b12 supplementation at the same time - consider testing if poor response seen
Pets often have low calcitriol levels in CKD - outline management of this
Evidence to suggest supplementation in dogs stage 3-4 increases lifespan
Before giving, ensure phosphate levels are in target levels and check i Ca
Outline management of proteinuria
Initiate therapy with a kidney diet and administer an angiotensin converting enzyme inhibitor (ACEI) with the therapeutic goal of reducing the UPC at least in half or, ideally, into the normal range
ACEi dilate the efferent arteriole, decreasing filtration pressure - a small number cannot cope with this leading to azotaemia
Benazepril has been advocated preferentially over enalapril because it is cleared largely by hepatic rather than renal excretion.
Start with once daily but often need twice daily
Occasionally ACE inhibitor therapy is associated with a marked decline in kidney function; therefore, serum creatinine should be measured before and 1–2 weeks after initiating therapy. If creatinine is more than 20% high, discontinue
May also lead to hyperkalaemia so monitor for this too
RC UPCR 1-3 after starting treatment
If an ACEi is not working, start ARB
Outline management of hypertension
ACEIs (eg, enalapril and benazepril) and calcium channel blockers (CCB; eg, amlodipine) are the preferred drugs
ACEI generally produce relatively small reductions in blood pressure, but have a beneficial role in altering intraglomerular hemodynamics, proteinuria, and the profibrotic effects of the intrarenal renin‐angiotensin system, ACEI may have renoprotective effects even when adequate arterial blood pressure control is not achieved.
When these aren’t effective, can try spironolactone, ARBs, atenolol, prazosin,
How is proteinuria related to prognosis?
Poorer if present
What is the typical disease found with CKD?
tubulointerstitial nephritis
Why does proteinuria cause disease progression
Not fully understood, could be
direct toxicity to tubular cells, inciting inflammatory responses or the formation of proteinaceous casts resulting in tubular obstruction.
Alternatively, may be the presence of other solutes that are filtered through a damaged glomerulus alongside protein that are damaging to the tubules.
How many cats with CKD will be proteinuric?
Approx 20%
Dogs likely more as glomerular dz more common
What is the structure of the glomerulus?
The glomerulus is a network of capillaries interposed between the afferent and efferent arterioles enclosed within an epithelial capsule (Bowman’s capsule) and separated by the Bowman’s space.
Glomerular filtration is a pressure-driven process governed by hydrostatic and oncotic pressures in the glomerular capillaries and Bowman’s capsule, and by glomerular conductivity and the capillary surface area.
It is charge and size selective
What makes up the filtration membrane?
fenestrated endothelial cells, basement membrane and podocytes
How does tubulointerstitial proteinuria occur
Tubulointerstitial proteinuria can develop as a result of defects in protein reabsorption in damaged renal tubular cells or a tubulopathy (eg, Fanconi syndrome) and is also likely to be exacerbated by accelerated tubular flow rates
How can you differentiate glomerula and tubular proteinuria
Mostly all just used in research and not fully confirmed
urine electrophoresis - small molecular weight in tubular, large in glomerular
Can guess a little with severity of UPC reading
How does high BP cause proteinuria
high systemic arterial pressure to the glomerulus. This in turn will increase hydrostatic pressure at the glomerular filtration barrier, resulting in the development of, or worsening of, pre-existing proteinuria. In addition, hypertension can contribute to renal injury.
What is the goal of treatment for BP
The goal of treatment should be a SBP between 120-150 mmHg in dogs and 120-160 mmHg in cats
What blood pressure drugs should be used in dogs?
Start with ACE inhibitor, if over 200 add in amlodipine to start with, otherwise add in if not a good enough response is seen
Where are the locations of possible proteinuria?
Prerenal proteinuria results from the inability of the tubules to reabsorb the high plasma content of small proteins that can freely pass across the glomerular barrier. Examples include immunoglobulin light chains in multiple myeloma, myoglobin in rhabdomyolysis and haemoglobin in intravascular haemolysis. Serum protein electrophoresis or other diagnostics are useful in excluding prerenal proteinuria.
Renal proteinuria results from glomerular or tubulointerstitial pathology. Functional proteinuria as a result of fever, seizure activity or strenuous exercise is possible, although it is rarely recognised in clinical patients.
Postrenal proteinuria results from the entry of proteins into the urine derived from exudative or haemorrhagic processes in the lower urinary tract or genital tract. Urine sediment examination should be performed to exclude postrenal proteinuria.
Aside from dispstick, what is another qualitative method of assessing proteinuria?
sulfosalicylic acid turbidimetric method - has to be sent to lab, assess with knowledge of SG and sediment, Finds albumin and globulin
A normal animal would be expected to have a UPC of <0.2 excpet in who?
intact male cat, the UPC may be less than 0.6,
