Tubular disorders of kidney Flashcards
By what age do puppies have full concentrating ability? What about kittens?
Puppies ~3 weeks
Kittens may not have full ability until 3 months of age
Other than colostral protein, what else is ‘abnormal’ about neonatal puppy and kitten urine?
Possible glucosuria in puppies due to immature PCT cells
Extremely dilute as dont have full concentrating ability yet
What is the normal USG for neonatal puppies and kittens?
1.006 - 1.007
What are the two major mechanisms of osmotic diuresis?
Overload of tubular resorptive capacity either due to
- increased concentration of the substance in the blood e.g diabetes, IMHA
- increased permeability of the glomeruli to the substance e.g glomerular amyloidosis
What is medullary washout? Give three diseases that might lead to this.
When filtrate flow rate is so fast that there is limited time for NaCl reabsorption in the LOH. Over time leads to electrolyte depletion in the medullary interstitium, and destroys the medullary concentration gradient. This reduces ability to concentrate urine. May occur in any disease that causes prolonged polyuria e.g diabetes insipidus, hypoadrenocorticism, Fanconi syndrome
What is the name for the high concentration of uric acid in Dalmation and english Bulldog urine? How much higher is it?
Hyperuricosuria - around 10 x higher
What might be a clue that a patient has primary renal glucosuria rather than diabetes mellitus?
They are normoglycemic
Their urine will contain glucose due to a defect in PCT reabsorption.
Name one tubular disease that could cause metabolic acidosis, and explain the mechanism
Fanconi syndrome - failure to reabsorb Na and Cl plus other solutes would cause both polyuria and medullary washout. Furthermore failure to reabsorb most HCO3- would cause acidosis.
Acidosis would be more mild in a condition where the only thing limiting tubular reabsorption was flow rate.
How severe is acute nephrosis? Why? How much urine do these patients produce?
Acute nephrosis is usually due to sudden hypoxia or toxic damage to renal tubules. Patients are anuric or oliguric, which leads to marked hyperkalaemia and potentially life threatening cardiac complications. Will die if not seen within ~ 3 days.
What are three gross lesions of acute nephrosis?
Streaking of cortex due to fatty +/- hydropic degeneration
Swollen, excessively wet kidney due to oedema
Petechial haemorrhages of capsule
What are three microscopic lesions of acute nephrosis?
Sloughing of cells into lumen > casts
Hydropic and fatty degeneration of tubular epithelium
Dilated tubules
Interstitial fibrosis in survivors
What characterises toxic nephrosis? Does it have a better or worse prognosis than hypoxic nephrosis usually?
Degeneration of tubular epithelial cells + preservation of tubular basement membrane. Better prognosis than hypoxic nephrosis, though hypoxic damage may be superimposed.
What is the name of the characteristic crystals that form in ethylene glycol toxicity?
Calcium oxalate monohydrate
What are the initial clinical signs in a dog or cat that has been poisoned by ethylene glycol?
Depression, polyuria and ataxia
Would also be hypocalcaemic
What is the general pathogenesis for interstitial nephrosis?
Haematogenous arrival of an infectious agent at the kidney, spread via the vasa recta to the interstitium to cause acute - chronic inflammation +/- abscesses
May lead to renal failure
Which structure is normally responsible for preventing retrograde urinary flow? What is special about this structure in puppies?
The vesicoureteral valve - ureters enter at a right angle in puppies as not fully developed, so predisposed
What are 5 factors that may promote urine reflux back up the ureters from the bladder?
Compromise of the vesicoureteral valves Narrowing of bladder outflow by exudate Oedema Uroliths Reverse peristaltic waves of the ureters due to endotoxin
What are the four reasons that the renal medulla is particularly vulnerable to infection?
- Relatively poor blood supply
- Low PCV of vasa recta blood
- Inhibition of complement by high ammonia concentration
- Impaired of leukocyte phagocytic activity by hypertonic environment
What pattern is typically seen in pig kidneys with pyelonephritis? Why?
Typically more severe at the poles
Compound papillae at the poles are more likely to remain patent when intrapelvic pressure is increased than the papillae toward the middle of the renal pelvis, which typically collapse in response. This prevents bacterial ascent, so bacteria typically progress into the parenchyma at the poles more easily.
What does scar formation due to the capsular surface of the kidney in chronic pyelonephritis?
Scars extend from the cortex to the medulla, so typically see dimpling and undulation of the cortex as they contract down and mature.
What is hypercalcaemic nephropathy?
High blood Ca2+ causing impaired renal tubular function and , later, metastatic mineralisation
What are some disease processes that can result in hypercalcemic nephropathy?
Paraneoplastic syndrome - secretion of PTHrP by anal sac adenocarcinoma or lymphoma
Primary hyperthyroidism
Hypervitaminosis D or poisoning with vitamin D analogue e.g cholecalciferol (Quintox rat bait)
Hypoadrenocorticism
What is the mechanism for hypercalcemic nephropathy?
High blood Ca2+ causes higher Ca2+ concentration inside cells, which activates adenylate cyclase inappropriately leading to reduced Na+ reabsorption in PCT and collecting duct
Also get impaired response to ADH
Get polyuria, natriuresis
If persists, get progressive metastatic mineralisation and loss of function
What is one parasite species that migrates through the kidneys in larval stage?
Toxicara canis = dog roundworm
Causes small cream-white granulomas in outer cortex
