Acute Renal Failure Clinical Presentation

A detailed and accurate history is crucial to the diagnosis of the type of acute kidney injury (AKI) that a patient has and to determining the disease’s subsequent treatment.

Distinguishing AKI from chronic renal failure is important, yet making the distinction can be difficult. A history of chronic symptoms—fatigue, weight loss, anorexia, nocturia, and pruritus—suggests chronic renal failure.

Take note of the following findings during the physical examination:

• Hypotension
• Volume contraction
• Congestive heart failure
• Nephrotoxic drug ingestion
• History of trauma or unaccustomed exertion
• Blood loss or transfusions
• Evidence of connective tissue disorders or autoimmune diseases
• Exposure to toxic substances, such as ethyl alcohol or ethylene glycol
• Exposure to mercury vapors, lead, cadmium, or other heavy metals, which can be encountered in welders and miners

People with the following comorbid conditions are at a higher risk for developing AKI:

• Hypertension
• Congestive cardiac failure
• Diabetes
• Multiple myeloma
• Chronic infection
• Myeloproliferative disorder

Urine output history can be useful. Oliguria generally favors AKI. Abrupt anuria suggests acute urinary obstruction, acute and severe glomerulonephritis, or embolic renal artery occlusion. A gradually diminishing urine output may indicate a urethral stricture or bladder outlet obstruction due to prostate enlargement.

Because of a decrease in functioning nephrons, even a trivial nephrotoxic insult may cause AKI to be superimposed on chronic renal insufficiency.

Acute kidney injury (AKI) has a long differential diagnosis. History can help classify the pathophysiology of AKI as prerenal, intrinsic renal, or postrenal failure, and it may suggest some specific etiologies.

Prerenal failure

Patients commonly present with symptoms related to hypovolemia, including thirst, decreased urine output, dizziness, and orthostatic hypotension.

Elders with vague mental status change are commonly found to have prerenal or normotensive ischemic AKI.

Ask about volume loss from vomiting, diarrhea, sweating, polyuria, or hemorrhage.

Patients with advanced cardiac failure leading to depressed renal perfusion may present with orthopnea and paroxysmal nocturnal dyspnea.

Insensible fluid losses can result in severe hypovolemia in patients with restricted fluid access and should be suspected in elderly patients and in comatose or sedated patients.

Intrinsic renal failure

Patients can be divided into those with glomerular etiologies and those with tubular etiologies of AKI.

Nephritic syndrome of hematuria, edema, and HTN indicates a glomerular etiology of AKI. Query about prior throat or skin infections.

ATN should be suspected in any patient presenting after a period of hypotension secondary to cardiac arrest, hemorrhage, sepsis, drug overdose, or surgery.

A careful search for exposure to nephrotoxins should include a detailed list of all current medications and any recent radiologic examinations (ie, exposure to radiologic contrast agents).

Pigment-induced AKI should be suspected in patients with possible rhabdomyolysis (muscular pain, recent coma, seizure, intoxication, excessive exercise, limb ischemia) or hemolysis (recent blood transfusion).

Allergic interstitial nephritis should be suspected with fevers, rash, arthralgias, and exposure to certain medications, including NSAIDs and antibiotics.

Postrenal failure

Postrenal failure usually occurs in older men with prostatic obstruction and symptoms of urgency, frequency, and hesitancy. Patients may present with asymptomatic, high-grade urinary obstruction because of the chronicity of their symptoms.

A history of prior gynecologic surgery or abdominopelvic malignancy often can be helpful in providing clues to the level of obstruction.

Flank pain and hematuria should raise a concern about renal calculi or papillary necrosis as the source of urinary obstruction.

Use of acyclovir, methotrexate, triamterene, indinavir, or sulfonamides implies the possibility of tubular obstruction by crystals of these medications.

Obtaining a thorough physical examination is extremely important when collecting evidence about the etiology of acute kidney injury (AKI).

Skin

Skin examination may reveal the following:

• Livido reticularis, digital ischemia, butterfly rash, palpable purpura - Systemic vasculitis
• Maculopapular rash - Allergic interstitial nephritis
• Track marks (ie, intravenous drug abuse) - Endocarditis

Petechiae, purpura, ecchymosis, and livedo reticularis provide clues to inflammatory and vascular causes of AK.

Infectious diseases, TTP, DIC, and embolic phenomena can produce typical cutaneous changes.

Eyes

Eye examination may reveal the following:

• Keratitis, iritis, uveitis, dry conjunctivae - Autoimmune vasculitis
• Jaundice - Liver diseases
• Band keratopathy (ie, hypercalcemia) - Multiple myeloma
• Signs of diabetes mellitus
• Signs of hypertension
• Atheroemboli (retinopathy)

Evidence of uveitis may indicate interstitial nephritis and necrotizing vasculitis.

Ocular palsy may indicate ethylene glycol poisoning or necrotizing vasculitis.

Findings suggestive of severe hypertension, atheroembolic disease, and endocarditis may be observed on careful examination of the eyes.

Ears

Ear examination may reveal the following:

• Hearing loss - Alport disease and aminoglycoside toxicity
• Mucosal or cartilaginous ulcerations - Wegener granulomatosis

Cardiovascular system

Cardiovascular examination may reveal the following:

• Irregular rhythms (ie, atrial fibrillation) - Thromboemboli
• Murmurs - Endocarditis
• Increased jugulovenous distention, rales, S₃ - CHF

The most important part of the physical examination is the assessment of cardiovascular and volume status.

The physical examination must include pulse rate and blood pressure recordings measured in the supine position and the standing position; close inspection of the jugular venous pulse; careful examination of the heart, lungs, skin turgor, and mucous membranes; and assessment for the presence of peripheral edema.

In hospitalized patients, accurate daily records of fluid intake and urine output and daily measurements of patient weight are important. Hypovolemia leads to hypotension; however, hypotension may not necessarily indicate hypovolemia.

Severe CHF may also cause hypotension. Although patients with CHF may have low blood pressure, volume expansion is present and effective renal perfusion is poor, which can result in AKI.

Severe hypertension with renal failure suggests renovascular disease, glomerulonephritis, vasculitis, or atheroembolic disease.

Abdomen

Abdominal examination may reveal the following:

• Pulsatile mass or bruit - Atheroemboli
• Abdominal or costovertebral angle tenderness - Nephrolithiasis, papillary necrosis, renal artery thrombosis, renal vein thrombosis
• Pelvic, rectal masses; prostatic hypertrophy; distended bladder – Urinary obstruction
• Limb ischemia, edema - Rhabdomyolysis

Abdominal examination findings can be useful to help detect obstruction at the bladder outlet as the cause of renal failure, which may be due to cancer or an enlarged prostate.

The presence of tense ascites can indicate elevated intra-abdominal pressure that can retard renal venous return and result in AKI.

The presence of an epigastric bruit suggests renal vascular hypertension, which may predispose to AKI.

Pulmonary

Pulmonary examination may reveal the following:

• Rales - Goodpasture syndrome, Wegener granulomatosis
• Hemoptysis - Wegener granulomatosis