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White crystals (uremic frost) and yellowish skin in CKD indicate severe uremia due to toxin accumulation from impaired kidney function. Applying medicated lotion addresses skin symptoms but does not treat the underlying uremia, which can lead to life-threatening complications like metabolic acidosis, hyperkalemia, or encephalopathy. This action is secondary to addressing systemic toxicity through dialysis.

A cardiac monitor detects arrhythmias, which may occur in CKD due to hyperkalemia or fluid overload. However, monitoring alone does not address the root cause of uremia. Without dialysis to correct metabolic imbalances, arrhythmias may persist or worsen, making this action less urgent than initiating dialysis to stabilize the patient’s condition.

Assessing a fistula for bruit and thrill ensures vascular access patency for dialysis. While important, it is not the priority when uremic symptoms are present, as dialysis orders must be secured first to address the acute uremic state and prevent life-threatening complications like encephalopathy or cardiac arrest due to toxin accumulation.

Urine output of 2000 mL in 24 hours indicates polyuria, characteristic of the recovery phase of AKI, not the oliguric phase, where output is typically less than 400 mL/day. High urine output suggests restored renal function, which is not expected in the oliguric phase, where kidneys fail to filter adequately.

Tachycardia may occur in AKI due to fluid overload causing increased cardiac workload or electrolyte imbalances like hyperkalemia affecting heart rhythm. However, it is a secondary symptom and less specific than hyperkalemia, which directly results from impaired renal excretion and poses a more immediate risk to cardiac function.

Tenting of the skin indicates dehydration, which may precede AKI but is not typical in the oliguric phase, where fluid retention is more common due to reduced urine output. Fluid overload leads to edema, not dehydration, making skin tenting an unlikely finding in this phase of AKI.

Advising increased fluid intake is incorrect for anuric ESRD patients, as their kidneys cannot excrete fluid. This would exacerbate fluid overload, leading to hypertension, heart failure, or pulmonary edema. Hydration is managed through dialysis, not increased oral intake, which could overwhelm the body’s limited fluid-handling capacity.

Stating that fluid intake is unrestricted with dialysis is incorrect. Even with regular dialysis, excessive fluid intake between sessions can lead to overload, causing hypertension or pulmonary edema. Dialysis removes a limited amount of fluid per session, requiring strict restrictions to maintain safe fluid balance and prevent complications.

While potassium and phosphorus restrictions are critical in ESRD to prevent hyperkalemia and hyperphosphatemia, the client’s question focuses on fluid restrictions. This response does not address fluid overload risks like hypertension or pulmonary edema, which are direct consequences of excessive fluid intake in anuric patients, making it irrelevant to the query.

Renal failure impairs erythropoietin production, a hormone stimulating red blood cell synthesis, leading to anemia, not an increased red blood cell count. Reduced glomerular filtration exacerbates toxin accumulation, further suppressing bone marrow activity, making an elevated red blood cell count unlikely in this condition.

In renal failure, kidneys fail to excrete potassium, leading to hyperkalemia, not decreased serum potassium. Hyperkalemia can cause cardiac arrhythmias due to altered membrane potentials. A decreased potassium level is more associated with conditions like diuretic use or vomiting, not renal failure.

Renal failure typically causes hypocalcemia, not increased serum calcium, due to impaired vitamin D activation and phosphate retention, which binds calcium. Hypercalcemia is rare and may occur in other conditions like hyperparathyroidism, not renal failure, where calcium homeostasis is disrupted by kidney dysfunction.

Antihypertensives are routinely used in ESRD to manage hypertension caused by fluid overload and renin-angiotensin system dysregulation. Controlling blood pressure prevents cardiovascular complications like heart failure or stroke, which are common in ESRD due to chronic volume and pressure overload, making this medication appropriate.

Erythrocyte-stimulating agents, like erythropoietin, are standard in ESRD to treat anemia caused by reduced erythropoietin production by failing kidneys. These agents stimulate red blood cell production, improving oxygen delivery and reducing fatigue, making them essential for managing ESRD-related anemia and improving quality of life.

Phosphate binders are used in ESRD to manage hyperphosphatemia by binding dietary phosphate in the gut, preventing its absorption. This reduces the risk of vascular calcification and secondary hyperparathyroidism, common complications in ESRD due to impaired phosphate excretion, making these medications a standard part of therapy.

Left-sided flank pain may suggest kidney stones or infection but is not specific to AKI. Pain can occur in various conditions, including pyelonephritis or ureteral obstruction, and does not directly indicate reduced glomerular filtration or oliguria, which are hallmarks of AKI, making it less urgent.

Blood pressure of 138/86 mm Hg and heart rate of 92 bpm are within normal ranges and not specific to AKI. While hypertension can occur in AKI due to fluid overload, these values do not strongly suggest AKI without other signs like oliguria or lab abnormalities.

Cloudy urine with sediment and foul odor suggests a urinary tract infection, not necessarily AKI. Infections can coexist with AKI but are not diagnostic. AKI is characterized by reduced urine output and elevated creatinine, not primarily by urine appearance, making this finding less indicative.

Taking blood pressure in the left arm with an AV fistula risks compressing the fistula, potentially causing thrombosis or damage. This can impair dialysis access, leading to inadequate treatment and complications like uremia or fluid overload. Blood pressure should be measured in the opposite arm to protect the fistula.

Keeping the AV fistula site dry is important to prevent infection, as moisture can promote bacterial growth. However, it is not the priority over ensuring fistula patency, which is critical for effective dialysis. Infection prevention is secondary to confirming the fistula’s functionality to avoid life-threatening dialysis interruptions.

Wrapping the AV fistula in gauze is not standard practice unless post-surgical or infected. Excessive wrapping may obscure the site, hindering patency assessments, and could increase infection risk if not changed properly. This action is less critical than ensuring the fistula’s functionality for dialysis.

Improved nutritional status could cause weight gain but is unlikely in AKI with minimal urine output. AKI patients often have anorexia or dietary restrictions, and weight gain from nutrition would not align with oliguria, which suggests fluid retention rather than increased tissue mass from improved nutrition.

A 3-pound weight gain in 48 hours with minimal urine output is clinically significant in AKI, indicating fluid retention. Normal weight fluctuations are minimal, and this rapid gain, coupled with oliguria, suggests impaired kidney function, potentially leading to fluid overload complications like hypertension or pulmonary edema.

Early AKI recovery involves increased urine output (diuresis phase), not minimal output. Weight gain with oliguria indicates ongoing kidney dysfunction, not recovery. Recovery would show improved glomerular filtration and urine production, reducing fluid retention, making this finding inconsistent with AKI recovery.

Increased potassium intake is dangerous in ESRD, as impaired kidneys cannot excrete potassium, leading to hyperkalemia. This can disrupt cardiac membrane potentials, causing arrhythmias or cardiac arrest. ESRD diets require strict potassium restriction to prevent life-threatening electrolyte imbalances, making this modification inappropriate.

Increased protein intake is often recommended in ESRD patients on hemodialysis to replace protein lost during dialysis and prevent malnutrition. However, it must be balanced to avoid excess urea production, which can worsen uremia. This is not the primary focus compared to phosphorus management in this context.

Decreased calcium intake is not recommended in ESRD, as patients often have hypocalcemia due to impaired vitamin D activation and phosphate retention. Calcium supplementation or adequate intake is needed to prevent bone disease and secondary hyperparathyroidism, making this modification incorrect for ESRD management.

Advancing the catheter further risks perforation or malposition, potentially damaging peritoneal tissues or organs. Slow drainage is often due to positional obstruction or constipation, not catheter depth. This invasive action requires medical orders and imaging confirmation, making it inappropriate as a first step in addressing slow drainage.

Infusing additional dialysate worsens abdominal distension and does not address slow drainage. It may increase intra-abdominal pressure, causing discomfort or complications like hernia. The issue is outflow obstruction, not insufficient dialysate, so adding more fluid is counterproductive and could exacerbate the client’s condition.

Aspirating with a syringe is not standard practice and risks introducing infection or damaging the catheter. It does not address underlying causes like positional obstruction or fibrin clots. Medical evaluation or specialized interventions like heparin instillation are needed for persistent drainage issues, making this action inappropriate.