Nephrology Notes PDF

Intravenous administration of normal saline prior to and for several hours after performing contrast-enhanced CT angiography is indicated in patients who are at risk of developing contrast-induced nephropathy. Major risk factors include chronic kidney disease, diabetes mellitus (particularly diabeti...

Intravenous administration of normal saline prior to and for several hours after performing contrast-enhanced CT angiography is indicated in patients who are at risk of developing contrast-induced nephropathy. Major risk factors include chronic kidney disease, diabetes mellitus (particularly diabetic nephropathy), dehydration, and the use of nephrotoxic drugs (e.g., NSAIDs). This patient\'s laboratory studies show elevated creatinine and borderline normal BUN level, which suggest impaired kidney function. Therefore, urgent prophylactic hydration is vital in this patient. Laboratory monitoring is necessary following the procedure to detect worsening creatinine levels (typically highest after 3-5 days), which would indicate contrast-induced nephropathy NSAIDs should be avoided prior to, and for several hours after, administering intravascular contrast medium because they cause renal vasoconstriction and subsequently increase the risk of contrast-induced nephropathy. Other nephrotoxic drugs (e.g., ACE inhibitors) should also be discontinued. - The first step in management pt with prerenal azotemia should be volume repletion with (isotonic fluid(normal saline ) or blood transfusion) - Prerenal azotemia can be secondary to diuretics. Diarrhoea. Blood loss - White cells and red cells seen in renal causes of AKI - Markedly elevated ratio of blood urea antigen to creatinine suggest prerenal azotemia (AKI) - Antithymocyte globulin is used to prevent acute rejection in transplant recipient - Intravenous glucocorticoids (methylprednisolone)is indicated for suspect or proven flare of lupus nephritis but it is unlikely in pt with normal compliment and inactive urine sediment - Pt with AKI regain full GFR after 2 weeks while tubular reabsorption remain impaired which result in increase urine production and polyuria (in which loss of several electrolytes happen( k lead to hypokalemia.na.mg) ) - Polyuria =loss of electrolyte in urine = decrease electrolyte from blood - Hypovolemia : dry mucous membrane.hypotension.tachycardia - Hypovolemia =hypoperfusion =prerenal AKI =BUN /CREATININE RATIO MORE THAN 20:1=intrinsic AKI (acute tubular necrosis. - Allergic interstitial nephritis (AIN) typically develops as a hypersensitivity response to certain drugs, most commonly PPIs, NSAIDs, antibiotics, and diuretics. AIN can also manifest with elevated levels of BUN and creatinine, and potentially result in AKI. However, additional features of AIN, such as flank pain, painless hematuria, and eosinophilia, are not present in this patient. In addition, AIN is an intrinsic cause of AKI, which is characterized by a BUN/creatinine ratio \< 15:1. - AKI: Prerenal :FENa LESS THAN 1% INTRINSIC :FENa MORE THAN 1% - Acute tubular necrosis (ATN), the most common aetiology of intrinsic acute kidney injury (AKI). It manifests with: oliguria, and laboratory values show elevated FeNa (typically \> 2%), a BUN:Cr ratio \< 15:1 in the absence of postrenal obstruction, and a low urine specific gravity (due to the inability to concentrate urine). Urine sediment usually shows epithelial cell casts (due to denudation of tubular basement membrane) or characteristic muddy brown granular casts. Proteinuria, if present, is typically in the non-nephrotic range (\< 3.5 g/dL/day). - nephritic syndrome is caused by inflammatory damage to the glomerular basement membrane, which leads to the leakage of red blood cells, and, in some cases, proteins. Laboratory studies typically show elevated BUN and creatinine levels, hematuria with red blood cell casts, a low specific gravity (due to the inability to concentrate urine), and non-nephrotic range proteinuria (\< 3.5 g/dL/day). - Nephrotic syndrome is a collection of disorders that result in damage to the glomerular filtration barrier. Urinalysis typically shows massive proteinuria (\> 3.5 g/24 hours) and fatty casts (due to elevated serum lipid concentration). - An increase of up to 30% in a patient\'s serum creatinine level upon initiation of an angiotensin-converting-enzyme inhibitor or an angiotensin II-receptor blocker is acceptable and is best managed by continuing the antihypertensive therapy. - (ACE) or (ARB), both of which have been shown to delay progression of renal disease. - Intravenous administration of isotonic fluid ( normal saline or sodium bicarbonate )prior to and for several hours after performing contrast-enhanced CT angiography is indicated in patients who are at risk of developing contrast-induced nephropathy. Major risk factors include chronic kidney disease, diabetes mellitus (particularly diabetic nephropathy), dehydration, and the use of nephrotoxic drugs (e.g., NSAIDs). This patient\'s laboratory studies show elevated creatinine and borderline normal BUN level, which suggest impaired kidney function. Therefore, urgent prophylactic hydration is vital in this patient. Laboratory monitoring is necessary following the procedure to detect worsening creatinine levels (typically highest after 3-5 days), which would indicate contrast-induced nephropathy. NSAIDs should be avoided prior to, and for several hours after, administering intravascular contrast medium because they cause renal vasoconstriction and subsequently increase the risk of contrast-induced nephropathy. Other nephrotoxic drugs (e.g., ACE inhibitors) should also be discontinued. - Acute tubular necrosis is the most common cause of intrinsic acute kidney injury (AKI), accounting for approx. 85% of cases. Prolonged hypotension in association with trauma and surgery significantly increases the risk of renal ischemia, which results in damage to and necrosis of the tubules. Subsequently, patients present with signs of AKI (e.g., oliguria, elevated BUN and creatinine). Renal epithelial cells and muddy brown granular casts that slough off in the tubular lumen are seen on urine microscopy. - The increase in sodium and water retention causes an increase in urine osmolality. - Patients with CHF being treated with loop diuretics should have renal laboratory values monitored because of the potential adverse effects on the kidney( due to volum depletion ) - Nephrotoxic drugs???? \- NSAID :ex : ibuprofen , naproxen, diclofenac -Aminoglycosides antibiotics (ex. Gentamicin, Tobramycin, Amikacin. ) -vancomycin -ACE ibibitors and ARBs -contrast agent \- Others \...ect - Muddy brown granular cast are specific to Acute tubular necrosis - RBCS cast indicate glomerulonrphtitis - WBCS CAST indicates pyelonephritis and acute interstitial nephritis - Fatty casts on urine microscopy are a characteristic finding in nephrotic syndrome. This manifests in massive proteinuria (\> 3.5 g/24 h), edema, and compensatory hyperlipidemia - Pigmented casts are a characteristic feature of AKI that occurs in the setting of rhabdomyolysis or hemolysis. - Hyaline casts are the most commonly observed casts in urine sediment analysis. Their presence is nonspecific. They are commonly seen in healthy individuals who have recently exercised vigorously or been dehydrated. - Membranous nephropathy is the most common cause of nephrotic syndrome in adults. Nephrotic syndrome is associated with acquired hypercoagulability due to urinary loss of proteins (e.g., antithrombin III) and thereby predisposes affected individuals to thrombotic complications such as renal vein thrombosis (RVT). MR venography is the diagnostic modality of choice in patients with AKI or renal impairment (eGFR \< 30 ml/min/1.73 m²). - While selective renal venography is the gold standard and CT angiography the diagnostic test of choice in patients with suspected acute bilateral RVT, both studies require iodinated contrast media, which would put this patient at risk for contrast-induced nephropathy. Other common causes of RVT include malignancy and trauma. - unilateral RVTs secondary to nephrotic syndrome are most commonly chronic, asymptomatic, and identified incidentally (e.g., during evaluation of a pulmonary embolism). - Low urine sodium is likely to be observed in cases of dehydration because it results in activation of the RAAS, which releases aldosterone from the adrenals to increase sodium reabsorption in the collecting ducts. This mechanism enables passive water reabsorption, which increases intravascular volume. - In the setting of volume depletion, the kidney can maintain glomerular filtration by prostaglandin-mediated vasodilation of the afferent arteriole and angiotensin II-mediated vasoconstriction of the efferent arteriole. However, if a patient take NSAIDs and continued taking his ACE inhibitor, which block these two autoregulatory defenses. In addition, pt taking diuretic, which can contribute further to the volume depletion. Taken together, these agents can produce acute kidney injury.( medication induced decrease in glomerular perfusion) - In the setting of volume depletion and the use of agents that block the renin-angiotensin-aldosterone axis, the use of nonsteroidal anti-inflammatory drugs can precipitate acute kidney injury. - Risk factors for contrast-induced acute kidney injury include chronic kidney disease, diabetes, heart failure, advanced age, volume depletion, hypotension, use of concurrent nephrotoxic medications, and use of a large-volume or high-osmolality contrast agent. - In addition to periprocedural intravenous fluid administration, the approach most likely to reduce the risk for contrast-induced nephropathy is use of a low-osmolar or iso-osmolar contrast agent. - This patient\'s presentation with diffuse muscle tenderness, highly elevated creatine kinase, and elevated lactate dehydrogenase is suggestive of muscle injury. These features together with darkened urine in the absence of RBCs on urinalysis indicate rhabdomyolysis, most likely due to overexertion as a result of the intensive training. - Acute kidney injury (AKI) is a common complication of rhabdomyolysis and crush syndrome. The excessive muscle breakdown results in increased free myoglobin and subsequent myoglobinuria (darkened urine without detectable RBCs). Pigments of heme-containing proteins, e.g., myoglobin or hemoglobin can harm the kidney tubules (= pigment nephropathy), causing acute tubular necrosis and subsequent AKI. Volume depletion secondary to third-spacing of fluid into the injured muscles leads to decreased renal perfusion and may thus further impair kidney function. - Patients with rhabdomyolysis require careful resuscitation with IV fluids and close monitoring of their urine output and electrolytes. Hemodialysis may be indicated in cases of severe AKI. Patients should also be monitored for compartment syndrome, as overly rapid fluid resuscitation can lead to increasing edema of the injured muscle and its adjacent compartment, potentially threatening its perfusion. - Most cases of postoperative oliguria are caused by decreased renal perfusion due to hypovolemia (resulting from intraoperative hemorrhage or insensible fluid losses) and renal afferent arteriole constriction (resulting from intraoperative catecholamine surge and increased sympathetic tone). The administration of intravenous crystalloid fluids (lactated Ringer\'s solution or normal saline) is the best next step in the management of a catheterized patient with postoperative oliguria and azotemia because increasing intravascular fluid volume via a fluid challenge will increase renal perfusion and thereby reverse these processes. - If the urine output does not increase after adequate fluid resuscitation, or if azotemia persists or worsens, a different cause of acute kidney injury (e.g., acute tubular necrosis, rhabdomyolysis, ongoing fluid losses, or, less likely, abdominal compartment syndrome) should be considered. - intrinsic kidney failure, which is typically caused by renal tubular or interstitial dysfunction (e.g., acute tubular necrosis, acute interstitial nephritis). Intrinsic AKI presents with elevated creatinine levels, a decreased BUN:Cr ratio (\< 15:1) due to decreased urea reabsorption, and impaired sodium reabsorption, causing a urine sodium concentration \> 40 mEq/L and urine osmolality \< 350 mOsm/kg. - prerenal azotemia, which can develop when the circulating intravascular volume is depleted or ineffective (e.g., in CHF), CHF leads to reduced renal blood flow, which stimulates the activation of the renin-angiotensin-aldosterone system. The release of aldosterone causes Na+ and water retention in an attempt to maintain GFR and systemic blood pressure, which in turn increases urea reabsorption (BUN:Cr ratio \> 20:1) and decreases the fraction of excreted Na+ (FENA + \< 1%). Increased Na and water retention cause elevated urine osmolality (\> 500 mOsm/kg) and urine specific gravity. Because of this potential adverse effect on the kidney, it is important to monitor renal laboratory values in patients with CHF. - postrenal azotemia, which is typically caused by urine outflow obstruction (e.g., benign prostatic hyperplasia, renal stones, neoplastic compression) and can lead to elevated creatinine levels and signs of urinary obstruction (e.g., bladder distention, urinary hesitancy) and/or flank or lower abdominal pain. Although serum and urinary studies can vary in postrenal azotemia because the tubular system continues to concentrate urine and filter sodium, urine osmolality is typically \< 350 mOsm/kg. - patient presents with symptoms of orthostatic syncope caused by hypovolemia (signs of dehydration), which was possibly worsened by a longer period of inactivity (watching TV) and her diuretic medication (hydrochlorothiazide). Orthostatic syncope due to hypovolemia can be confirmed by elevated blood urea nitrogen concentrations (BUN concentrations) and an elevated BUN/creatinine ratio, which are caused by renal hypoperfusion Prerenal injury reflects a functional decrease in perfusion of the kidney, but the renal parenchyma is intact. This can occur from volume depletion (as from gastrointestinal losses, blood loss, or third spacing) or effective volume depletion (as in congestive heart failure or cirrhosis). Restoration of perfusion will promptly improve kidney function. - Intrinsic or parenchymal renal injury can result from damage to the glomeruli, tubules, or interstitium. Tubular damage can occur from ischemic damage to the kidney (as with prerenal injury but without restoration of perfusion) or from toxins. -. Prerenal injury and ischemic damage to the tubules (also called acute tubular necrosis) may occur in the same clinical circumstances. Restoration of perfusion with intravenous fluids can distinguish between the two conditions because prerenal injury will improve rapidly. - isotonic fluids, such as normal saline or lactated Ringer solution. - The appropriate initial fluids for a patient with volume depletion and acute intrinsic renal injury are isotonic fluids administered at 10 to 20 mL/kg. - 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 and angiotensin-receptor blockers should be held because these agents interfere with glomerular autoregulation and can also lead to hyperkalaemia. - IN pt with AKI due to acute tubular necrosis with no evidence of volume depletion(euvolemic ) and the pt on ACEI and ARB medication the next step is to hold taking this medication - Contrast-induced nephropathy is a cause of toxic ATN and a common cause of inpatient AKI. This condition should be suspected if a hospitalized patient develops intrinsic AKI and had an indication for intravascular administration of radiographic contrast media (e.g., abdominal CT with IV contrast for the diagnosis of acute diverticulitis, angiography for the management of cardiac chest pain). Patient-related risk factors for contrast-induced nephropathy include advanced age, diabetes mellitus, underlying chronic kidney disease (CKD) such as diabetic nephropathy, and concomitant use of certain nephrotoxic drugs (e.g., NSAIDs). The creatinine levels peaking after 3-5 days and returning to baseline within one week. - Measures to prevent contrast-induced nephropathy include adequate hydration with isotonic fluids before and after administration of contrast medium, avoidance of ionic and hyperosmolar contrast media, the use of contrast media at the lowest possible dose, and, if possible, discontinuing nephrotoxic substances before contrast administration. - \.... - Costovertebral angle tenderness, burning on urination, fever, and leukocytosis in conjunction with positive nitrite and pyuria on urinalysis are suggestive of acute pyelonephritis. - Pregnant women with acute pyelonephritis are require hospitalization and treatment with parenteral broad-spectrum antibiotics; third-generation cephalosporins (e.g., cefotaxime) are considered safe for this patient group. Medication can be switched to oral antibiotic therapy according to the results of culture susceptibility tests. - features of dehydration (agitation, confusion, lethargy, prolonged capillary refill time) and hypernatremia with a low urine osmolality indicate severe diabetes insipidus (DI). Additionally, her recurring headaches, visual impairment, and recent seizure raise suspicion of a brain tumor. - An underlying neurological disorder (e.g., a brain tumor such as craniopharyngioma or metastasis) can lead to direct or indirect dysfunction of the hypothalamic neurons of the posterior pituitary gland, which causes decreased ADH secretion and consequently, central DI. Central DI may be idiopathic or secondary; other secondary causes include traumatic brain injury, pituitary bleeding, subarachnoid hemorrhage, pituitary ischemia, meningitis, and neurosurgery. - DI is confirmed via the water deprivation test, which would show no change in urine osmolality despite a rising plasma osmolality. After DI is confirmed, desmopressin is administered to distinguish between central or nephrogenic DI. A subsequent increase in urine osmolality after a desmopressin trial indicates intact ADH receptors in the kidneys, confirming central diabetes insipidus. - IgA nephropathy most commonly manifests with recurrent episodes of gross hematuria(intermittent bloody urine ), flank pain, low-grade fever, and/or nephritic syndrome, usually during or immediately following (within days) an upper respiratory tract infection. Between these episodes, patients typically have asymptomatic urinary abnormalities, such as microhematuria. The most likely etiology of these findings is an increased number of defective circulating IgA antibodies, the synthesis of which is triggered by mucosal infections (e.g., pharyngitis). These IgA antibodies form immune complexes that deposit in the mesangium of the renal glomerulus, leading to glomerulonephritis (type III hypersensitivity reaction). A renal biopsy provides a definitive diagnosis but is usually only indicated if there are signs of severe or progressive disease (e.g., proteinuria \> 0.5-1 g/24 h, hypertension, elevated creatinine levels). Renal biopsy would show mesangial immune complex deposits on electron microscopy. -