NSAIDS induced renal disease

Severe kidney damage was linked with the production of all the non-steroidal anti-inflammatory medications (NSAIDs).

Acute kidney failure due to NSAIDs

Two forms of severe kidney failure may be triggered by NSAIDs.

• Hemodynamically induced (e.g. pre-renal and/or severe necrosis of the tubes).
• Mediated immune response (e.g. severe interstitial nephritis).

Acute kidney injury is a process of renal disease that occurs from clinically-asymptomatic renal function improvements to renal dysfunction and death. A significant kidney injury has been characterized by a gradual decrease over hours to days in the rate of glomerular filtration (GFR).

Diagnosis and Analysis

The acute kidney damage caused by NSAID does not display any clear signs or symptoms. Acute kidney injury signs can be non-specific to the skin which can involve shortness of breath, exhaustion, discomfort, nausea.
The signs of volume depletion may occur in patients who suffer from pre-renal injury including-:

• Tachycardia
• Absolute or postural hypotension
• Low jugular venous pressure
• Dry mucous membranes.

Interstitial nephritis patients may have systemic hypersensitivity characteristics including arthralgia, fever, and a pruritic-erythematous rash. There might also be eosinophilia.

Factors of pathology and risk

The inhibition of COX-1 and COX-2 of NSAIDs can reversibly inhibit the formation of renal prostaglandins. Full inhibition exists in steady amounts, plasma concentrations.
The dilation of renal afferent arteriole is caused by renal prostaglandins. The function is important when GFR production is decreased (i.e. not in young healthy people). It is crucial for preserving GFR. The use of NSAID in patients with other risk factors is therefore likely to have a greater effect on renal function.
The effects of acute interstitial Nephritis on NSAIDs are unclear. However, cyclooxygenase hemming has been suggested to contribute to preferential arachidonic acid conversion into leukotrienes which could then activate T-helper cells.

Risk factors for NSAID induced acute kidney injury

Risk factor	Effect
Chronic hypertensive and atherosclerotic age (particularly age > 65).	Renal arterioles reduction that may reduce their ability to dilate the renal afferent.
Glomerular or renal insufficiency pre-existing	Renal afferent dilatation is probably necessary for GFR maintenance.
Decline in volume Depletion of true volume (i.e., salt or renal or loss of water, blood loss, diuretic use) Effectively decreasing volume (such as cirrhosis and cardiac insufficiency)	Reduces glomerular arteriolar pressure and enhances angiotensin II secretion
Application of ACE or ARB inhibitors.	ACE and ARB inhibitors prevent afferent vasoconstriction of arteriole which is also significant in maintaining GFR.
The ‘triple whammy’ (ACE or ARB plus NSAID diuretic)	Diuretic can cause a decrease in volume.

• ACE is explained as an Angiotensin Converting Enzyme;
• ARB is described as Angiotensin II Receptor Blocker

The most important risk factors for experiencing acute renal injury are pre-existing severe kidney disorder and increased age.

Treatment

After the withdrawal of NSAID therapy, renal function will recover in most patients. In interstitial nephritis patients with stopped NSAID therapy, steroids may help recovery. For these cases, the potential usage of NSAIDs will be discouraged.