Cutaneous And Renal Glomerular Vasculopathy Research Articles

Helping practitioners to stop the rot.

Rare and often fatal, cutaneous and renal glomerular vasculopathy (CRGV) has attracted much interest since the first UK cases were identified a decade ago. At BVA Live, David Walker will be sharing his knowledge of the disease with the aim of helping practitioners understand when CRGV should be high on their list of differential diagnoses.

Cerebral Microangiopathy in Two Dogs with Cutaneous and Renal Glomerular Vasculopathy

Cutaneous and renal glomerular vasculopathy (CRGV) is an emerging disease in the UK, but its aetiology remains unclear. It is considered a thrombotic microangiopathy (TMA) in which the kidney and skin are the most commonly affected organs. We now document two cases of CRGV with brain lesions, which may have accounted for neurological signs displayed by these animals. The histopathological brain lesions were similar to TMA lesions in humans with thrombotic thrombocytopaenic purpura (TTP) and complement-mediated haemolytic uraemic syndrome (CM-HUS), in which the neurological signs are more associated with TMA than with any systemic disease or electrolyte imbalance. Fibrinoid necrosis in brain arterioles and associated lesions in these dogs were similar to those in human CM-HUS, indicating that the alternative complement pathway may play an important role in the pathophysiology of CRGV.

Clinicopathological features of cutaneous and renal glomerular vasculopathy in 178 dogs.

One hundred seventy-eight dogs with cutaneous and renal glomerular vasculopathy (CRGV) were evaluated to further the understanding of the natural course of CRGV. CRGV, a form of thrombotic microangiopathy, can cause skin lesions and potentially acute kidney injury (AKI) with a high mortality rate. Cases were submitted from multiple practices from 2012 until June 2019. Clinical histories and laboratory data were reviewed to describe the features of CRGV. Most cases (91%) occurred between November and May. Fifteen dogs (8.4%) with CRGV were in contact with another dog that developed skin lesions +/- AKI. Limb lesions were present on 144 dogs (80.9%) at presentation. Median time from appearance of a lesion to AKI was 3 days (range -4-45 days). Neurological signs occurred in 33 dogs (18.6%) including at presentation in 2 (1.1%). Systemic signs were present in 13 dogs prior to a skin lesion (7.3%). Non-steroidal anti-inflammatory drugs were prescribed prior to AKI identification in 92 of 170 dogs (54.1%). Thrombocytopenia was present in 115 of 137 (83.9%) of dogs. The timeframe over which AKI may develop is longer than previously reported, neurological signs can be identified at presentation or during hospitalisation, and thrombocytopenia is even more common than previously reported.

Pathology and Epidemiology of Cutaneous and Renal Glomerular Vasculopathy in Dogs

Cutaneous and renal glomerular vasculopathy (CRGV) has been recognized as a potentially life-threatening condition of dogs in the UK since 2012, although there was a single (non-azotaemic) case reported in the UK in 2000. Prior to that, CRGV was recognized in the 1980s in southern USA as a disease affecting solely racing greyhounds (which gave rise to the colloquial name of 'Alabama rot'). CRGV manifests as ulcerative skin lesions, generally sparing the dorsum. It is variably associated with systemic signs including anaemia, thrombocytopenia and acute kidney injury, which, when it develops, is often severe and fatal. CRGV is characterized histopathologically as a thrombotic microangiopathy. To date in the UK, more than 230 dogs of varying breed and age have been humanely destroyed and histopathologically confirmed to be suffering from CRGV. The aetiology remains unknown, but the seasonal distribution (highest case incidence November-May each year) suggests that environmental or climatic factors may play a role in disease development. Further research to determine the aetiology and improve ante-mortem diagnostic testing, therapeutic options and preventive strategies is urgently needed.

Dealing with cutaneous and renal glomerular vasculopathy in dogs

Cutaneous and renal glomerular vasculopathy (CRGV) is a disease of dogs, first reported in racing greyhounds in the USA during the 1980s. The disease causes erosive to ulcerative skin lesions,...

Teasing out the risks for Alabama rot

Cutaneous and renal glomerular vasculopathy (CRGV) – more commonly known as Alabama rot – was first reported in the UK in 2012. Since then cases have been reported annually. The...

Spatiotemporal patterns and agroecological risk factors for cutaneous and renal glomerular vasculopathy (Alabama Rot) in dogs in the UK

The annual outbreaks of cutaneous and renal glomerular vasculopathy (CRGV) reported in UK dogs display a distinct seasonal pattern (November to May) suggesting possible climatic drivers of the disease. The...

Description of the Use of Plasma Exchange in Dogs With Cutaneous and Renal Glomerular Vasculopathy.

Cutaneous and renal glomerular vasculopathy (CRGV) is a rare disease affecting dogs, with a recent apparent increase in prevalence since 2012 in the UK. This disease is characterized by a vasculopathy affecting small vessels of the kidney and skin, leading to thrombotic microangiopathy. The underlying etiology remains unknown although clinicopathological and histological findings resemble features of certain forms of thrombotic microangiopathy in people, for which plasma exchange (PEX) is considered an important component of therapy. The objective of the present study is to describe the use of PEX as adjunctive treatment in dogs diagnosed with CRGV. A retrospective review of dogs diagnosed with CRGV between 2014 and 2016 treated with PEX was performed. Clinical records were reviewed and data relating to signalment, diagnostic tests and management strategies were summarized. Information and complications relating to PEX were recorded. Six dogs were diagnosed with CRGV (n = 2 ante-mortem, n = 4 post-mortem) and underwent PEX as part of their therapy. All dogs had cutaneous lesions and were azotemic with oliguria or anuria. All dogs underwent at least one PEX cycle; one dog had a single cycle PEX, three dogs two cycles PEX, and two dogs had one cycle PEX and one cycle of prolonged intermittent renal replacement treatment. Complications seen during PEX therapy included hypothermia (n = 4), tachycardia (n = 2), hypotension (n = 2), and hypocalcemia (n = 6). Two dogs survived to discharge, the remaining four dogs were euthanized. The positive outcome in two dogs treated with PEX despite the reported high mortality rate once acute kidney injury with oliguria/anuria occurs does not confirm success of this treatment. However, survival in two dogs that were initially oligoanuric highlights that further consideration and evaluation of PEX for this patient group is warranted for this specific disease. Additional studies are urgently needed to identify the underlying etiology of CRGV before more targeted therapies can be developed. Based on our findings, further evaluation of the role of PEX in this specific disease are warranted.

‘New Forest syndrome’: first pieces of the puzzle

IN THE past two to three years, there has been much interest surrounding the apparent emergence of a disease commonly known to the general public as ‘New Forest syndrome’. There...

Cutaneous and renal glomerular vasculopathy as a cause of acute kidney injury in dogs in the UK

To describe the signalment, clinicopathological findings and outcome in dogs presenting with acute kidney injury (AKI) and skin lesions between November 2012 and March 2014, in whom cutaneous and renal...

Glomerular ultrastructural lesions of idiopathic cutaneous and renal glomerular vasculopathy of greyhounds.

Idiopathic cutaneous and renal glomerular vasculopathy (CRGV) (Alabama rot) is a potentially fatal disease of unknown etiology that affects the skin and kidneys of racing- and training-age Greyhounds. Ultrastructural examinations were performed on two healthy control Greyhounds and 12 Greyhounds diagnosed with CRGV based on the presence of characteristic, well-demarcated cutaneous ulcers of the extremities (12/12), thrombocytopenia (< 200,000 platelets/dl) (12/12), and acute renal insufficiency (BUN > 40 mg/dl, serum creatinine > 2.0 mg/dl) (7/12). Early glomerular ultrastructural changes included endothelial swelling, detachment, and necrosis; membranous whorl formation; and platelet adhesion and aggregation. Some capillaries were occluded with aggregated platelets, cellular fragments, and fibrin. Later changes included narrowing of capillary lumina and thickening of glomerular capillary walls by subendothelial accumulation of flocculent, amorphous, variable electron-dense material and occasionally erythrocytes, cellular processes, and fibrin. Glomerular endothelial cells were increased in number and plump, with villouslike cytoplasmic projections. Mesangial cell cytoplasmic processes occasionally were interposed between the endothelium and the basement membrane. No etiologic agents or electron-dense deposits typical of immune complexes were observed. Although the specific etiology was not determined, the ultrastructural changes suggest that glomerular endothelial damage is an important early event in the pathogenesis of CRGV.