- Urinary problems (1◦ or 2◦)
- Genitourinary problems (vaginal or urethral discharge)
- Systemic problems e.g. dehydration, ascites, edema, vomiting, oral ulceration, osteodystrophy, depression, coma.
- Confirm the problems and, as far as possible, reach as specific a diagnosis as possible.
- Localise the problems: urinary (prerenal, renal or postrenal) vs. Extra-urinary
- Urinary tract disease may be localised as either lower urinary tract, glomerular, tubular
- Azotemia may be prerenal, renal or postrenal.
- PU-PD may be related to renal disease or endocrine diseases such as diabetes mellitus, diabetes insipidus and hyper- or hypoadrenocorticism (see the list above).
- Inflammatory cells or bacteria in urine may relate to either the urinary or genital systems.
- Use the information obtained 1 & 2 to plan an appropriate treatment and management plan.
AZOTEMIA + CLINICAL SIGNS
- Azotemia = ↑ serum urea +/- creatinine
- Clinical signs have multiple causes which include accumulation of compounds normally filtered by the kidneys: e.g. urea, creatinine, ammonia, uric acid, leucine, tyrosine, sulphates, phosphates, chloride, potassium, organic acids (acidosis and increased anion gap are often associated with RF).
- The gastrointestinal tract is severely affected; vomiting occurs in carnivores, oral and GI ulceration, diarrhea, constipation, "uremic" or ammoniacal breath.
- Gastrin is a digestive hormone that causes the stomach to secrete acid. It is excreted by the kidneys and gastrin levels rise with renal insufficiency resulting in increased gastric acidity, nausea and other gastrointestinal signs.
- The central and peripheral nervous systems are affected causing depression (most species) and peripheral neuropathy .'. neurological signs
- Anemia often occurs in chronic renal failure (because kidney is responsible for Epo production
- Osteopathy (renal osteodystrophy) may also develop
- Synthesised in the liver
- Small quantities are ingested/absorbed from large intestine
- Hepatic urea cycle synthesis urea from ammonia - the waste product of protein catabolism
- Not found in the faeces
- Appears in the glomerular filtrate in the same concentration as in the plasma
- As it passes along the renal tubules it diffuses passively according to concentration gradients and membrane permeability (influenced by AVP/ADH in the CD).
- Not reabsorbed as efficiently as water
- Rate of reabsorption is related to the rate of flow through the tubules;
1. ↑ rates of urine flow =↓ reabsorption
2. ↓ rates of urine flow = ↑ reabsorption.
- Partially reabsorbed in the DT
- Anything that ↓ the GFR will↑ the blood urea.
- Processes which induce protein catabolism can increase urea production: hemorrhage into the small intestine, fever, burns, corticosteroids, starvation, infection.
- ↑ nitrogen intake in ruminants significantly ↑ urea synthesis in the liver leading to development of mild, prerenal azotemia.
- ↓ urea synthesis may occur with ↓ protein intake or severe hepatic insufficiency.
- Chronic polyuria may result in a ↓ blood urea (washout effect) .'. rate of reabsorption is inversely related to the rate of flow through the tubules
- Urea can be measured in serum, some plasmas and urine
- Some references refer to BUN (blood urea nitrogen); if using SI units this does not affect interpretation, but if converting from mg/dL to SI units it is important to use the correct conversion factor .'. ↑BUN = ↓GFR
- The assay is quite robust and between run CV is expected to be < ≈4.0% with lower values having a CV closer to the upper end of this range.
- Influenced by the diet
- Azostix reagent test strips can be used to get an estimate of the BUN.
1. Useful for ruling out azotemia as they are effective at detecting "normal" blood urea concentrations, but they tend to underestimate value
2. Very low sensitivity, but high specificity
- To determine the fraction of material filtered that appears in urine (sodium, calcium, potassium, chloride, phosphorus)
- Reflects the efforts of the kidney to maintain homeostasis or defects in its ability to do so.
- Requires concurrent urine and blood samples
- Those electrolytes/substances that are conserved (e.g. Na, Cl) have very low FCR values (0 - 4%) while K and P have higher values (20 - 50%)
- Values are affected by diet as well as time since last meal; this is more important in carnivores where food intake is less constant than in herbivores.
- Uses include:
- The diagnosis of primary hyperparathyroidism (increased FCR-P, but direct measurement of PTH is becoming more common),
- Monitoring of renal secondary hyperparathyroidism (increased FCR-P, decreased FCR-Ca) in CRF cases,
- diagnosis of tubular dysfunction (eg increased FCR-Na)
- FCR based on spot measurements should be done after a 12 to 15 hours fast because dietary intake and intestinal absorption can affect the results. Ideally, feed a standardised diet for several days before the sample is collected.
- Measurement of any FER requires collection of a urine sample followed immediately by collection of a blood sample