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Erythropoietin, produced by the kidneys, stimulates red blood cell production in bone marrow. It does not directly influence GFR, which is determined by renal blood flow and pressure. In pre-renal AKI, reduced cardiac output decreases renal perfusion, impairing filtration. Erythropoietin levels may decrease in AKI, but this is a consequence, not a cause, of reduced GFR, making this option incorrect.

Dihydroxy vitamin D, activated by the kidneys, regulates calcium and phosphate for bone health. It does not directly affect GFR, which depends on hemodynamic factors like blood flow. In pre-renal AKI, reduced perfusion, not vitamin D metabolism, causes GFR decline. This option is incorrect as it does not relate to the primary mechanism of GFR reduction.

The glomerular capillary wall, comprising endothelium, basement membrane, and podocytes, forms the filtration barrier. While it facilitates filtration, GFR is primarily driven by blood flow and pressure, not the wall’s structure. In pre-renal AKI, reduced cardiac output decreases perfusion, not the capillary wall’s integrity, causing GFR reduction, making this choice incorrect.

Cystitis is bladder inflammation, typically from bacterial infection, affecting the lower urinary tract. Nephrotoxins like antibiotics or snake venom target renal parenchyma, causing intra-renal AKI, not cystitis. Cystitis leads to urinary symptoms like dysuria but does not impair renal filtration or cause AKI, making this option incorrect for nephrotoxin-related kidney injury.

Pyelonephritis is a kidney infection, often ascending from the urinary tract, caused by bacteria like E. coli. While it can cause AKI, it is not the primary mechanism of nephrotoxin-induced injury. Nephrotoxins directly damage renal tubules, leading to ATN, not infection-based inflammation, so pyelonephritis is not the most accurate choice.

Hydronephrosis is kidney swelling due to urine outflow obstruction, causing pressure-related damage. Nephrotoxins cause direct cellular injury, leading to ATN, not obstruction. Hydronephrosis results from mechanical issues like stones or tumors, not toxic insults, making this option incorrect for intra-renal AKI caused by nephrotoxins.

Testicular heaviness and cryptorchidism (undescended testes) are unrelated to post-renal AKI, which results from urinary tract obstruction. Cryptorchidism affects testicular development and may increase cancer risk but does not obstruct urine flow or cause AKI. This option is incorrect as it does not align with post-renal AKI pathophysiology.

Oliguria (low urine output) can occur in post-renal AKI due to obstruction, but hypertension is not a direct cause or typical historical factor. Hypertension may contribute to pre-renal or intra-renal AKI by damaging vessels or glomeruli but is less specific to post-renal causes, making this choice less accurate.

Elevated serum creatinine indicates kidney dysfunction, including AKI, but polycystic kidney disease primarily causes intra-renal AKI through cystic damage to renal tissue. Post-renal AKI requires obstruction, not intrinsic renal damage, so this option is incorrect as it does not reflect the obstructive etiology of post-renal AKI.

Autoantibodies, formed in response to streptococcal antigens, cross-react with glomerular basement membranes, causing immune-mediated damage. This triggers inflammation, impairing glomerular function and reducing GFR. This immune response is a hallmark of post-streptococcal GN, contributing to its pathophysiology, making this a correct feature of the condition.

Inflamed glomeruli become permeable, allowing red blood cells and proteins to leak into the urine, causing hematuria and proteinuria. This pathological leakage results from damaged glomerular capillaries, a key feature of post-streptococcal GN, contributing to clinical manifestations like cola-colored urine, making this a correct feature.

Inflammatory changes, driven by immune complex deposition in glomeruli, cause capillary damage, increasing permeability. This leads to leakage of blood and proteins into the urine and reduced GFR. Inflammation is central to post-streptococcal GN’s pathophysiology, making this a correct feature of the disease process.

CKD typically causes metabolic acidosis, not alkalosis, due to impaired acid excretion and reduced bicarbonate production. The kidneys normally reabsorb and generate bicarbonate to maintain acid-base balance, but in CKD, this function is compromised, leading to acidosis, making metabolic alkalosis an incorrect complication.

Hypophosphatemia is not a typical CKD complication; instead, hyperphosphatemia occurs due to reduced phosphate excretion. While CKD patients may have bone disease increasing fracture risk, hypophosphatemia is not the primary cause. Hip fractures are more related to altered calcium metabolism, making this choice incorrect.

Nephrolithiasis (kidney stones) is not directly caused by hypocalcemia in CKD. CKD often leads to hyperphosphatemia and altered calcium metabolism, but stones are more associated with hypercalcemia or other factors like hyperoxaluria. Hypocalcemia is a consequence, not a cause, making this choice incorrect.

A blood urea nitrogen (BUN) level of 6 mg/dL is within or below normal range (7-20 mg/dL) and does not indicate renal failure. In renal failure, BUN is elevated due to reduced kidney clearance of urea, a waste product. Normal or low BUN does not correlate with symptoms like altered mental status or pruritus, making this incorrect.

Hypercalcemia is not typical in renal failure; hypocalcemia is more common due to reduced vitamin D activation and phosphate retention. Hypercalcemia could cause neurological symptoms but is less likely in CKD and does not directly explain anorexia or pruritus, making this choice incorrect.

Urine specific gravity of 1.028 is within normal range (1.002-1.030) and reflects the kidneys’ ability to concentrate urine. In renal failure, this ability is impaired, often resulting in isosthenuria (normal range gravity despite dysfunction). This does not directly correlate with the symptoms, making it incorrect.

Chronic kidney disease is characterized by progressive renal damage, often with reduced urine output and isosthenuria (specific gravity near 1.010). A specific gravity of 1.029 and 40 ml output suggest concentrated urine, not typical of CKD’s early stages, where kidneys lose concentrating ability, making this choice incorrect.

Overhydration dilutes urine, lowering specific gravity (closer to 1.002). A specific gravity of 1.029 and low output (40 ml) indicate concentrated urine, typical of reduced fluid intake or loss, not excess fluid. Overhydration would increase urine volume and dilute solutes, making this choice incorrect.

A urine specific gravity of 1.029 is within the normal range (1.002-1.030), but 40 ml of urine is low, suggesting reduced output. While the specific gravity is normal, the low volume points to dehydration, not just a normal state, as clinical context matters, making this choice less accurate.

Alopecia is not a universal symptom of CKD. CKD causes symptoms like fatigue, edema, and uremia due to toxin accumulation and impaired filtration, not hair loss. Hair plugs address cosmetic issues unrelated to renal pathophysiology, making this an incorrect and irrelevant treatment option for CKD management.

CKD typically causes hyperphosphatemia, not hypophosphatemia, due to reduced phosphate excretion. Antacids may bind phosphate to lower levels, not increase them. Hypophosphatemia is rare in CKD and not treated with antacids, which are used for acid-base balance or dyspepsia, making this choice incorrect.

While dehydration can occur, CKD patients often have fluid overload due to impaired excretion, causing edema. Poor skin turgor and high serum osmolality suggest dehydration, but CKD treatment focuses on fluid balance, not routine hydration, as excess fluid worsens hypertension and edema, making this choice incorrect.

Retrograde menstruation is a theory for endometriosis, not ovarian cancer. It involves menstrual tissue flowing backward into the pelvis, causing ectopic endometrial growth. Ovarian cancer arises from malignant transformation of ovarian cells, unrelated to menstruation, making this an incorrect explanation for the disease’s etiology.

While diet may influence cancer risk, a high-saturated-fat diet is not a well-established primary risk factor for ovarian cancer. Genetic mutations (e.g., BRCA), hormonal factors, and family history are stronger contributors. This makes the dietary link less specific and incorrect as a primary cause explanation.

Annual Pap smears detect cervical cancer, not ovarian cancer. Ovarian cancer lacks effective screening tests, and Pap smears do not identify ovarian abnormalities. Early detection relies on imaging or biomarkers, not Pap smears, making this an incorrect statement for explaining ovarian cancer development.

Benign prostatic hyperplasia affects the prostate in males, causing urinary symptoms like hesitancy or frequency, not vaginal discharge or pelvic pain. It is irrelevant to female patients and does not cause gynecological symptoms, making this an incorrect choice for the patient’s presentation.

Kidney stones cause flank pain, hematuria, or colicky pain radiating to the groin, not constant pelvic pain or vaginal discharge. They affect the urinary tract, not reproductive organs, and are unrelated to the gynecological symptoms described, making this an incorrect diagnosis.