Laura Holm of Anderson Moores Vet Specialists wrote “Noticing signs of CRGV in dogs to diagnose disease presence” in the Vet Times (March 21st 2016).
Laura Holm said that only a quarter of dogs with skin lesions go on to get acute kidney injury:
“Evidence suggests the median time from the onset of a skin lesion, to development of azotaemia [high blood Nitrogen levels], is 3 days (range 0 to 10 days) … There does, however, appear to be a subset of dogs that develop skin lesions without azotaemia (non-azotaemic CRGV) … with about 75% of cases remaining systemically well following development of skin lesions and only about 25% developing clinical signs attributable to AKI [Acute Kidney Injury].”
Blood clots result in skin ulcers and kidney failure:
“When microthrombi [small blood clots] occlude [obstruct] blood supply in dermal [an area below the skin] vessels, dermal cell death occurs and cutaneous ulceration [skin ulcers] develops, whereas microthrombi in the glomeruli [kidney capillaries] reduce glomerular blood supply and glomerular filtration rate, potentially causing azotaemia [high nitrogen levels in blood] and oliguria [production of small amounts of urine] or anuria [failure of kidneys to produce urine].”
Of the 75% dogs that have skin ulcers without kidney injury, the prognosis is excellent. Of the other 25% of dogs that have skin lesions and kidney injury, 85% die when treated at vets whilst slightly fewer (75%) die when treated at referral centres [eg Anderson Moores Vet Specialists in Winchester]:
“For CRGV cases that remain non-azotaemic [normal blood nitrogen levels], the prognosis is excellent. Although skin lesions may take weeks or months to heal, a full recovery should be expected. Unfortunately, the prognosis is significantly less favourable in dogs with CRGV that develop AKI. Overall, more than 85% of CRGV cases with azotaemia have been euthanised or died… The outlook may be slightly better for cases managed in referral centres. Approximately 25% of azotaemic-suspected CRGV cases managed in referral centres have survived. However, no single therapy has been used more commonly in surviving cases and this figure is likely to reflect the more intensive monitoring and management generally possible in the referral setting.”
Laura Holm says that CRGV has not been reported in species other than dogs but CRGV-like diseases do occur in humans:
In humans a group of diseases exist that are characterised by thrombotic microangiopathy (TMA) [blood clots inside blood vessels] which bear some similarities to CRGV, namely: haemolytic uraemic syndrome (HUS) [anemia caused by destruction of red blood cells, acute kidney failure, and low platelet counts], atypical haemolytic uraemic syndrome (aHUS) [uncontrolled activation of the complement immune system that removes foreign particles] and thrombotic thrombocytopenic purpura (TTP) [microscopic clots that form in the small blood vessels].
But even in humans, the causes of CRGV-like diseases are poorly understood:
“Even in humans, the aetiopathogeneses [cause] of TMA illnesses are still relatively poorly understood. Definitive diagnosis can be challenging and treatment is not always successful.”
Reported by Chris Street BSc MSc at Alabamarot.co.uk (May 26th 2016)
Text in [ ] is by alabamarot.co.uk