Renal disease: chronic kidney disease Flashcards
Chronic kidney disease refers to
● Structural and/or functional abnormalities of one or both kidneys that have been continuously present for ≥3 months.
● Is irreversible and progressive
● Concurrent prerenal/postrenal azotemia, “acute-on-chronic” kidney disease.
● More common in older animals
Causes of chronic kidney disease.
● Initial inciting cause of CKD is not usually determined, likely a series of renal
insults.
Causes of chronic kidney disease in dogs. (4-5)
● Familial, congenital, acquired conditions
● Juvenile nephropathy (renal dysplasia) - young dogs
● Tubulointerstitial nephritis - older dogs
● Glomerular disease - majority
- Immune-complex mediated glomerular nephritis, amyloidosis, non-immune complex glomerulonephritis conditions, infectious diseases (borreliosis, ehrlichiosis, anaplasmosis, babesiosis, leishmaniasis)
Causes of chronic kidney disease in cats. (2)
● Tubulointerstitial nephritis
- Age, viral infection, extrarenal diseases, environmental factors,
ischemia, hypoxemia
● Polycystic kidney disease (PKD)
In the context of kidney disease, what important question should not be forgotten during anamnesis?
potential toxin exposure (lilies, pest bait and poisons etc.)
Clinical signs in potential chronic kidney disease patients.
● Can be subclinical in early stage
● PU/PD, weight loss, decreased appetite, lethargy, dehydration, vomiting, halitosis
Physical exam findings in potential chronic kidney disease patients.
● Normal in early stage
● Later: palpable kidney abnormalities (e.g. unilateral compensatory hypertrophy), evidence of weight loss, dehydration,
pale mucous membranes, uremic ulcers, evidence of hypertension (retinal hemorrhages/detachment).
CKD - findings persistent, no pre/postrenal causes
For the diagnosis of chronic kidney disease, hematological changes.
anemia
CKD - findings persistent, no pre/postrenal causes
For the diagnosis of chronic kidney disease, blood biochemical changes. (7)
Azotemia,
SDMA,
hyperP,
hypo/hyperK,
hypo/hyperCa,
hypoalb,
metabolic acidosis
CKD - findings persistent, no pre/postrenal causes
For the diagnosis of chronic kidney disease, urine-analytical changes. (9)
Impaired urine concentration/dilution,
proteinuria,
cylindruria,
hematuria,
pyuria,
inappropriate urine pH,
inappropriate urine glucose,
cystinuria,
bacteriuria
CKD - findings persistent, no pre/postrenal causes
For the diagnosis of chronic kidney disease, imagine diagnostics may show what types of changes?
Abnormal renal size, shape,
echotexture, mineralization,
uroliths, absence of a kidney,
neoplasia
CKD - findings persistent, no pre/postrenal causes
Diagnosis of chronic kidney disease stage 1 and early stage 2
One or more of these findings should be present:
● Creatinine/SDMA increasing within the reference interval where no prerenal
cause is apparent.
● Persistent increased SDMA >14 µg/dL
● Abnormal kidney imaging
● Persistent renal proteinuria
● UPC >0.5 in dogs,
>0.4 in cats
Diagnosis of chronic kidney disease late stage 2-4.
Both of these diagnostic findings must be present:
● Increased creatinine and SDMA concentrations
AND
● USG <1.030 in dogs, <1.035 in cats
Describe staging of chronic kidney disease.
● Only once the diagnosis has been confirmed and the patient is stable.
● For developing treatment plan and establishing prognosis.
● IRIS Guidelines
Based on renal function:
● Creatinine
● SDMA
Substages based on:
● Proteinuria
● Arterial blood pressure
(as seen in attached table)
Treatment of chronic kidney disease.
● Medical management is to minimize metabolic complications, slow progression.
● Treatment is individualized based on stage of disease and
- Clinical and laboratory status of the patient
- Owner
● Is a progressive and dynamic disease and therapy modifications are based on serial
clinical and laboratory assessment.
CKD-MBD, RSHP stand for:
CKD-MBD = Chronic kidney disease–mineral bone disorder
CKD-RSHP = Chronic kidney disease-refractory secondary hyperparathyroidism
Treatment of CKD-MBD, RSHP options. (4)
Dietary PO4 restriction
Phosphate binders
Cinacalcet
Calcitriol?
Describe Dietary PO4 restriction
● Therapeutic goal based on the IRIS CKD stage
● PO4 assessed after 12 h fast
● PO4 rechecked after 4-6 weeks
● When in Target range: continue renal diet, check PO4 q3-6m
● When phosphate Not in the target range: add intestinal binding agent
Describe Phosphate binders
● Aluminum hydroxide, Ca based, lanthanum salts, sevelamer carbonate.
● Give With renal diet
● At or around meal time
● Dosed to effect, adjust q2-4w
● If necessary, add a binding agent with a different mechanism of action
● Ineffective in anorectic patients
● Unpalatable
● Avoid Ca based with hyperCa, calcification, avoid giving with calcitriol. Monitor ionizedCa.
renal osteodystrophy caused by
caused by disturbances in mineral metabolism that occur as a result of kidney dysfunction.
- In CKD, the kidneys lose their ability to excrete phosphorus properly. High phosphorus levels cause a reduction in blood calcium levels, leading to an increase in parathyroid hormone (PTH) secretion, a condition called secondary hyperparathyroidism.
- Diseased kidneys cannot efficiently convert vitamin D into its active form, calcitriol, which is necessary for calcium absorption from the intestines.
- secondary hyperparathyroidism is a compensatory response to the low blood calcium and high phosphorus levels. Over time, the parathyroid glands become overactive and produce excessive PTH, which causes excessive bone resorption.
- The imbalance in calcium and phosphorus metabolism causes alterations in bone structure and strength, leading to fibrous osteodystrophy and osteomalacia.
Most common phosphate binder product.
oral suspension pronefra (binds phosphate from food, not from in body)
Pronefra® is delicious and based on the interaction of four ingredients.
- calcium carbonate and magnesium carbonate bind phosphorus in the digestive tract, reducing its absorption;
- chitosan is known as a binder of uremic toxins in the digestive tract;
- oligopeptide of marine origin helps to maintain normal blood pressure.
Describe the use of Cinacalcet for the treatment of CKD-MBD, RSHP.
● Is a Calcimimetic, meaning it mimics the action of calcium on tissues. It reduces PTH secretion and serum Ca.
● Risk of hypoCa when using it.
● 0.5 mg/kg q24h, increased q2-3w until PO4 and Ca are controlled/max 3 mg/kg
● Well tolerated but common side effects include Nausea, vomiting.
Treatment of uremia?
Diet: Decreased protein has been speculated for this but isn’t backed by adequate evidence.
Some suggest it has to do with protein quality instead.
dysrexia =
abnormal appetite
Treatment of CKD related: dysrexia, nausea, vomiting, weight loss, cachexia (4)
Esomeprazole, sucralfate
● When Clinical suspicion of GI ulceration
Maropitant, ondansetron
● Uremic nausea and vomiting
Mirtazapine, capromorelin (both appetite stimulants)
● Decreased appetite, weight loss
Esophagostomy feeding
● Patients that continue to lose weight despite all efforts to achieve adequate nutrition.
Treatment of CKD related dehydration
● Canned instead of dry food
● Adding water to food
● Fresh, accessible water always avail.
SubCut balanced electrolyte solutions
● but PO/feeding tube preferred
● In Cats that are prone to secondary complications of chronic dehydration (constipation) and do not suffer quality of life concerns from the procedure.
● 75-150 ml SC q1-3d depending on IRIS stage and clinical need.
● Frequent assessment: hydration status, clinical signs, BP, kidney function, blood electrolytes.
Treatment of CKD related constipation.
● Correction of dehydration
● Correction of hypoK
After correction of dehydration and hypoK:
● Osmotic stool softeners (like lactulose & Mg+)
● Promotility agents (cisapride)
● Medical management of osteoarthritis (cat more willing to poop when not painful)
Treatment of CKD related hypoK.
● Diets supplemented with K (cats)
● Oral K supplementation (product Kaminox)
- K gluconate, K citrate
● IV fluids supplemented with K chloride
- Hypokalemic myopathy (weakness, ventroflexion)
- Iatrogenic deficiency (IV fluid therapy during uremic crisis)
If Refractory to supplementation, consider hyperaldosteronism? NB cats can also have CKD and hyperaldosteronism which complicates things further!
Main 2 blood sample changes in hyperaldosteronism?
hypokalemia, <3.0mEq/L
hypernatremia but this can also be normal
(+ of course elevated aldosterone)
Treatment of CKD related arterial hypertension.
Indication:
● BP >200 mmHg and/or evidence of TOD (target organ damage e.g. eye lesions)
● BP consistently >160 mmHg
Goal: BP <150 mmHg
Cats (monotherapy):
● Amlodipine (Ca channel blocker)
● Telmisartan (ARB = angiotensin II receptor blocker) - not if TOD/BP >200 mmHg
Dogs (combination):
● ACEi
● Telmisartan
● Amlodipine
Later stages/uremic crisis -> amlodipine safer.
Monitoring Treatment of CKD related arterial hypertension.
Monitoring:
● Stable mildly hypertensive patient: BP within 7-10 days and the dose adjusted accordingly.
● Unstable, target organ damage/TOD, late stage disease: earlier (1-3 days).
● BP, renal values, electrolytes q3-6k
- Hypotension
- Worsening azotemia with ACEi/ARB (= angiotensin II receptor blocker)
- HyperK with ACEi (dogs)
Treatment of CKD related proteinuria.
● UPCR >0.5 in dogs, >0.4 in cats
● Antiproteinuric drugs are the same that we use for hypertensive patients.
- ACEi
- ARB (= angiotensin II receptor blocker)
● Antithrombotic therapy (glomerular disease)
● Treatment of systemic hypertension
● Diet? Theory about decreased protein content but this isn’t confirmed with evidence.
● Kidney biopsy to rule out immune mediated disease.
Treatment of CKD related anemia.
● Treat underlying conditions
e.g. GI hemorrhage can be cause.
- Melena, increased BUN to creatinine ratio, iron deficiency, anemia disproportionate to level of azotemia.
- Proton pump inhibitors
● Infections
● Chronic inflammation
● Some may even need Blood transfusion.
Describe Darbepoetin alfa.
For the treatment of CKD induced anemia.
● Erythrocyte-stimulating agent
● Based on human EPO - risk of developing antibodies.
● Indication: IRIS CKD III-IV + PCV <25% + clinical anemia
● 1 mcg/kg SC q1w until PCV 28-35% in cats, 37-42% in dogs, then q2w, maintenance dose adjusted q4w as needed.
● + iron dextran 50 mg/cat, 10-20 mg/kg dogs IM when treatment is initiated, then every few months through the course of therapy.
● + B vitamins
● Monitoring: Physical Exam, PCV, BP q1w until target PCV is reached (2-8 w), then q1-3m.
Treatment of CKD related metabolic acidosis.
● Treatment decision based on acid-base status.
- check Blood bicarbonate, pH
● Renal diet may be enough.
● K citrate/Na bicarbonate
- Small doses frequently to minimize blood pH fluctuations.
- Goal: blood bicarbonate WRI
- Recheck after 10-14 days before the drug is given, dosage adjusted accordingly.
Review IRIS treatment recommendations for CKD -table.
Monitoring CKD progression.
● Monitoring Frequency depends on severity of renal dysfunction, complications, treatments, response to treatment.
● q2-4w initially
● Dogs and cats in stage I CKD q6-12m
● Cats in stage II CKD q3-6m
● Dogs in stage II, dogs and cats in stage III
CKD q2-4m
● EPO/calcitriol - frequent monitoring
Prognosis for CKD.
● Variably progressive disease
● Many factors
● Slower progression in Cats and dogs that have congenital/familial nephropathies not characterized by proteinuria.
● First treat prerenal, postrenal, and active complications, IRIS CKD stage once the
patient is stable.
Median survival times
● Cats: 1151 d in stage II, 679 d in stage III, 35 d in stage IV.
● Dogs: 226 d. Stage III 2.6 times and stage IV 4.7 times the mortality compared with stages I and II.
● 14.8 m in stage II, 11.14 m in stage III, 1.98 m in stage IV.
Review checklist for managing CKD.
Surgical options for CKD? (2)
● Perinephric pseudocysts
● Kidney transplantation
