Salt losing nephritis is a feature of -
Interstitial nephritis
Renal amyloidosis
Lupus nephritis
Post streptococcal glomerulonephritis
Acute interstitial nephritis Acute interstitial nephritis (AIN) is an immune-mediated disorder, characterised by acute inflammation affecting the tubulo- interstitium of the kidney. It is commonly drug-induced, with proton pump inhibitors (PPIs) fast becoming the most common cause, but can be caused by other toxins, and can complicate` a variety of systemic diseases and infections . Clinical features The clinical presentation is typically with renal impairment but, in some patients with drug-induced AIN, there may be signs of a generalised drug hypersensitivity reaction with fever, rash and eosinophilia. Proteinuria is generally modest (PCR < 100 mg/mmol) and tubular in type ). The urine may contain white blood cells and white cell casts but is sterile on culture. Eosinophils are present in up to 70% of patients but this is a non-specific finding. AIN should` always be considered in patients with non-oliguric AKI. There` `may be a rapid deterioration of renal function in some cases of drug-induced AIN, causing the condition to be mistaken for RPGN. Investigations Renal biopsy is usually required to confirm the diagnosis . This typically shows evidence of intense inflammation, with infiltration of the tubules and interstitium by polymorphonuclear leucocytes and lymphocytes. Eosinophils may also be observed, especially in drug-induced AIN. Often granulomas may be evident, especially in drug-induced AIN or sarcoidosis . The degree of chronic inflammation in a biopsy is a useful predictor of long-term renal function. Eosinophiluria may be present but is not a good discriminator for AIN. Management Some patients with drug-induced AIN recover following withdrawal of the drug alone, but high-dose glucocoicoids (prednisolone 1 mg/kg/day) may accelerate recovery and prevent long-term scarring. Other specific causes should be treated, if possible. Chronic interstitial nephritis Chronic interstitial nephritis (CIN) is characterised by renal dysfunction with fibrosis and infiltration of the renal parenchyma by lymphocytes, plasma cells and macrophages, in association with tubular damage. Ref Harrison20th edition pg 299
Kidney