Dr. Richard Quigg is a nephrologist practicing in Willowbrook, IL. Dr. Quigg specializes in the care and treatment of the kidneys. As a nephrologist, Dr. Quigg most typically treats conditions like kidney stones, chronic kidney disease, acute renal failure, polycystuc kidney disease, high blood pressure and more. Nephrologists are also experts on kidney transplantation and dialysis. They are usually referred to by primary care physicians for problems related to the kidneys, and while they can perform tests to diagnose kidney disorders, they do not perform surgeries.
- Renal, central nervous system and pancreatic overexpression of recombinant soluble Crry in transgenic mice. A novel means of protection from complement-mediated injury.
- We need to inhibit complement in glomerular proteinuria.
- Predictors of early post-cardiac transplant exercise capacity.
- Production and functional analysis of rat CD59 and chimeric CD59-Crry as active soluble proteins in Pichia pastoris.
- Echocardiographic Doppler evaluation of left ventricular diastolic filling in older, highly trained male endurance athletes.
- Complement is activated in kidney by endotoxin but does not cause the ensuing acute renal failure.
- Expression of a soluble complement inhibitor protects transgenic mice from antibody-induced acute renal failure.
- A protein with characteristics of factor H is present on rodent platelets and functions as the immune adherence receptor.
- Accuracy of estimating exercise prescription intensity in patients with left ventricular systolic dysfunction.
- Inhibiting the complement system does not reduce injury in renal ischemia reperfusion.
- Value of the Bruce protocol to determine peak exercise oxygen consumption in patients evaluated for cardiac transplantation.
- Glomerular complement regulation is overwhelmed in passive Heymann nephritis.
- Injury in renal ischemia-reperfusion is independent from immunoglobulins and T lymphocytes.
- Transgenic expression of a soluble complement inhibitor protects against renal disease and promotes survival in MRL/lpr mice.
- A complement-dependent model of thrombotic thrombocytopenic purpura induced by antibodies reactive with endothelial cells.
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