Contrast-Induced Nephropathy Prevention

• Intravenous normal saline administration is indicated for patients at risk of contrast-induced nephropathy, especially after contrast-enhanced CT angiography.
• Risk factors for contrast-induced nephropathy include chronic kidney disease, diabetic nephropathy, dehydration, and nephrotoxic drugs like NSAIDs.
• Elevated creatinine and borderline normal BUN levels can indicate impaired kidney function, necessitating urgent prophylactic hydration.
• Laboratory monitoring for creatinine levels is crucial after contrast procedures to detect worsening kidney function, typically peaking within 3-5 days.
• NSAIDs can cause renal vasoconstriction, increasing the risk of contrast-induced nephropathy, so avoid before and after contrast medium administration.
• Discontinue other nephrotoxic drugs such as ACE inhibitors to manage prerenal azotemia via volume repletion with isotonic fluids or blood transfusion.
• Prerenal azotemia can stem from diuretics, diarrhea, or blood loss.
• The presence of white and red cells suggests renal causes of AKI.
• A markedly elevated blood urea nitrogen to creatinine ratio suggests prerenal azotemia (AKI).
• Antithymocyte globulin is used to prevent acute rejection in transplant recipients.
• Intravenous glucocorticoids like methylprednisolone treat lupus nephritis flares but are unlikely to help with normal complement and inactive urine sediment.
• AKI patients can regain full GFR after 2 weeks, but impaired tubular reabsorption can cause increased urine production and polyuria, leading to electrolyte loss.
• Polyuria indicates electrolyte loss in urine, resulting in decreased blood electrolytes; potassium can lead to hypokalemia causing symptoms like dry mucous membrane, hypotension, and tachycardia.
• Hypovolemia leads to hypoperfusion, resulting in prerenal AKI with a BUN/Creatinine ratio greater than 20:1, characteristic of intrinsic AKI or acute tubular necrosis.
• Allergic interstitial nephritis (AIN) is a hypersensitivity response to drugs, including PPIs, NSAIDs, antibiotics, and diuretics, which can elevate BUN and creatinine, potentially resulting in AKI.
• Flank pain, painless hematuria, and eosinophilia are additional features of AIN, AIN is an intrinsic cause of AKI, with a BUN/creatinine ratio < 15:1

AKI Subtypes

• Prerenal AKI: FENa is less than 1%.
• Intrinsic AKI: FENa is more than 1%.

Acute Tubular Necrosis (ATN)

• The most common etiology of intrinsic AKI is characterized by oliguria and elevated FeNa (typically > 2%).
• ATN also presents with a BUN:Cr ratio < 15:1 without postrenal obstruction, and low urine specific gravity due to impaired concentration.
• Urine sediment may show epithelial cell casts or muddy brown granular casts; proteinuria, if present, is typically in the non-nephrotic range (< 3.5 g/dL/day).

Nephritic Syndrome

• Nephritic syndrome is caused by inflammatory damage to the glomerular basement membrane and leads to leakage of red blood cells and proteins.
• It presents with elevated BUN and creatinine, hematuria with red blood cell casts, low specific gravity ,and non-nephrotic range proteinuria of < 3.5 g/dL/day.

Nephrotic Syndrome

• Nephrotic syndrome has several disorders, which result in damage to the glomerular filtration barrier.
• Urinalysis shows massive proteinuria (> 3.5 g/24 hours) and fatty casts (due to elevated serum lipid concentration).
• A serum creatinine increase of up to 30% upon initiating an ACE inhibitor or angiotensin II-receptor blocker is normally acceptable and best managed by continuing the antihypertensive therapy as delaying disease progression has been proven.
• Intravenous isotonic fluid prior to contrast-enhanced CT angiography is indicated for patients at the risk of nephropathy. Risk factors being chronic kidney disease, advanced age or diabetic mellitus and nephrotoxic drugs such as NSAIDs etc.
• This patient's laboratory studies show elevated creatinine and borderline normal BUN level, which suggest impaired kidney function.
• Urgent prophylactic hydration is vital for such patient.

Further Details on Managing Kidney Issues

• Monitoring for creatinine levels is necessary following the procedure to detect worsening creatinine levels.
• Avoid NSAIDs before and several hours after intravascular contrast medium administration to prevent renal vasoconstriction and increased the risk of nephropathy.
• Acute tubular necrosis is the most common cause of acute kidney injury as prolonged hypertension in association with major surgery increases risk of renal ischemia. Resulting in the damage and necrosis of tubules plus signs of AKI and epithelial cells with muddy brown granular cells.
• Increased sodium retention increases the urine osmolality.
• CHF patients treated with loop diuretics should have renal laboratory values monitored because of the potential adverse effects of volume depletion.
• Nephrotoxic drugs include examples such a NSAIDs, Aminoglycosides antibiotics , vancomycin , ACE inhibitors and ARBS and contrast agents.
• Muddy brown granular cast means Acute tubular necrosis whereas RBCS cast is associated with glomerulonrphtitis. WBCS signals for Acute interstitial nephritis, while Fatty indicate nephrotic syndrome.
• Hyaline casts are common found in healthy individuals due to vigorous exercise.
• Membranous nephropathy is the most common cause of nephrotic syndrome in adults associated with acquired hypercoagulability due to loss of protein.
• Renal vein thrombosis (RVT) is a thromboembolic condition and the diagnostic of choice being MR venography with creatinine levels less than 30 ml/min/1.73m2.
• Selective renal venography is the gold standard and CT angiography the diagnostic test in the event of suspected acute bilateral RVT requiring iodinated contrast media.
• Unilateral RVTs secondary to nephrotic syndrome are most commonly chronic, asymptomatic, and identified incidentally in an evaluation of pulmonary embolism.

Sodium-Regulated Mechanisms & Dehydration

• Low urine sodium means dehydration which activates the RAAS which uses aldosterone from adrenals to passive water reabsorption which increases intravascular volume.
• In setting of volume depletion , kidneys maintain glomerular filtration by prostaglandin mediated vasodilation and Angiotensin II -mediated vasoconstriction.
• Risk factors for Acute kidney injury due to contrasts also consider kidney/heart disease, diabetes, heart failure, advanced age, volume depletion/hypotension.
• The best way to reduce contrast-induced nephropathy is us of a low-osmolar or iso-osmolar contrast agent.
• Diffuse muscle tenderness paired with creatine kinase and elevated lactate dehydrogenase , indicates rhabdomyolysis in resultance with darkened une.

Understanding AKI Complications & More

• excessive muscle breakdown causes rhabdomyolysis and crush syndrome , which also causes myoglobinuria due to heme-containing proteins.
• Kidney tubules are causes of volume depletion due to the accumulation of third space fluids of injured muscles which leads to decreased renal perfusion. Patients with rhabdomyolsis are requires careful resuscitation of output and electrocytes, possibly hemodialysis.

Fluid Replacement

• First step in catheterized patients wit postoperative oliguria need intravenous cystalloid fluids to increase renal perfusion, may indicate different failure if no improvement occurs
• acute or chronic tubular kidney failure is cause by acute/chronic Interstitial Nephritis causing elevation of cretinine levels and decreased reabsorption levels.
• preneral azotemia depletes both intracellular and extracellular fluids which stimulates vasoreceptors.
• Decrease osmolality increase sodium causes body to maintain GFR.
• Post renal azotemia can be caused by outflow obstruction which varies with the the location and can be confirmed by urinary anaylisis and lab results.
• Patient shows orthostatic syscope confirmed by elevated (BUN) due too renal hypoperfusion as well as the use of diruetics.
• Volume and kidney failure may indicate restoration of perfusion so renal damage is intact.
• Tubular damage from ischemia due to toxins.

In Summary

• Intrinsic or parenchymal injury occur as ischemic damage due obstructions.
• Isotonic fluids such as lactated Ringer solution are often required for volume depletion. The need of them should be administered in limited quantities though.
• Treatment of acute tubular injury that results from ischemia or nephrotoxic agents is conservative, with a focus on supportive care including avoidance of exposure to further renal insults.
• Angiotensin-converting-enzyme inhibitors interfere with glomerular autoregulation and may result in hyperkalemia
• ACEI and ARB is best held at the first sign of renal tubulosis for kidney regulation.
• Contrast means acute injury of ATN and should be suspected if kidney failure for IV is caused by radiographic media.

Recognizing Acute Kidney Injury (AKI) & Understanding DI

• AKI occurs from patient factors such a diabetic neuropathy, nephrotic drugs requiring to measure cretinine levels and fluid management.
• Costovertebral angle tenderness shows acute pyelonephritis which requires to hospitalization and broad antibiotic medicine.
• Dehydration can be recognize from agitation and recurring headaches due to brain tumors.
• Hypothalamic neurons dysfunction also affect the posterior pituarity glands as well the ADH resulting in the DI, which is confirmed by a water testing
• Water testing shows the change between Urine and Plasma , needing to be confirmed by kidney.
• recurring episodes of hematuria(intermittent bloody urine ) is an IgA Nephropathy which requires direct upper Respiratory and needs IgA antibodies with protein greater is requires a complex kidney transplant.

Managing contrast-induced nephropathy risk involves intravenous normal saline for at-risk patients undergoing contrast-enhanced CT angiography. Key risk factors include chronic kidney disease and nephrotoxic drugs like NSAIDs. Monitoring creatinine levels and discontinuing nephrotoxic medications is crucial for prevention.