Pulmonary-renal syndrome (PRS) is a rare medical syndrome in which respiratory failure involving bleeding in the lungs and kidney failure (glomerulonephritis) occur. PRS is associated with a high rate of morbidity and death. The term was first used by Goodpasture in 1919 to describe the association of respiratory and kidney failure. Causes
Pulmonary-renal syndromes are most commonly caused by an underlying autoimmune disease. PRS is most commonly due to ANCA-associated vasculitides (e.g., granulomatosis with polyangiitis) or due to anti-basement membrane diseases (e.g., Goodpastures syndrome). Granulomatosis with polyangiitis usually presents with nasopharyngeal involvement as well, whereas Goodpastures will not. Microscopic polyangiitis is the most common cause of pulmonary-renal syndrome.Other causes include systemic lupus erythematosus, eosinophilic granulomatosis with polyangiitis, microscopic polyangiitis, dermatomyositis, polymyositis, mixed connective tissue disease, poststreptococcal glomerulonephritis, rheumatoid arthritis, and systemic sclerosis. Less common causes also include IgA vasculitis and cryoglobulinemic vasculitis. Other etiologies include toxic injury such as paraquat poisoning, infection with hantavirus, leptospirosis, or legionella, or vascular, as seen in nephrotic syndrome when a renal vein thrombosis embolizes to the lungs. Diagnosis
Differential diagnosis
Cardiogenic shock can mimic a pulmonary renal syndrome and lead to coughing up blood due to pulmonary edema and kidney failure from inadequate blood flow. Treatment
Treatment is primarily by corticosteroids and immunosuppressive medications like cyclophosphamide, methotrexate, and azathioprine. Plasmapheresis can be used in some circumstances. == References ==
Although standard doses used to treat psychosis inhibit dopaminergic neurotransmission, low doses preferentially block inhibitory presynaptic autoreceptors. This results in a facilitation of dopamine activity, and for this reason, low-dose amisulpride has also been used to treat dysthymia.Amisulpride and its relatives sulpiride, levosulpiride, and sultopride have been shown to bind to the high-affinity GHB receptor at concentrations that are therapeutically relevant (IC50 = 50 nM for amisulpride).Amisulpride, sultopride and sulpiride respectively present decreasing in vitro affinities for the D2 receptor (IC50 = 27, 120 and 181 nM) and the D3 receptor (IC50 = 3.6, 4.8 and 17.5 nM).Though it was long widely assumed that dopaminergic modulation is solely responsible for the respective antidepressant and antipsychotic properties of amisulpride, it was subsequently found that the drug also acts as a potent antagonist of the serotonin 5-HT7 receptor (Ki = 11.5 nM). Several of the other atypical antipsychotics such as risperidone and ziprasidone are potent antagonists at the 5-HT7 receptor as well, and selective antagonists of the receptor show antidepressant properties themselves. To characterize the role of the 5-HT7 receptor in the antidepressant effects of amisulpride, a study prepared 5-HT7 receptor knockout mice. The study found that in two widely used rodent models of depression, the tail suspension test, and the forced swim test, those mice did not exhibit an antidepressant response upon treatment with amisulpride.