Angela, A 24-Year-Old Female, Felt Swollen, Weak, And Fatigu

Angela Was A 24 Year Old Female Felt Swollen Weak And Fatigued For S

Angela Was A 24 Year Old Female Felt Swollen Weak And Fatigued For S

Angela was a 24-year-old female who experienced swelling, weakness, and fatigue over several months. She noticed her urine had a red-brown discoloration and was low in volume, prompting her to seek emergency medical attention. Examination and laboratory tests revealed abnormal hematology, urinalysis, and renal function parameters. In this essay, we will analyze Angela’s clinical presentation, identify her likely disorder, explore potential causes, and discuss pertinent renal and electrolyte abnormalities.

Paper For Above instruction

Angela’s presentation of swelling, weakness, fatigue, and hematuria is indicative of a renal disorder affecting kidney function and electrolyte balance. Her laboratory findings, including hyponatremia, hyperkalemia, elevated serum creatinine, reduced glomerular filtration rate (GFR), and abnormal urinalysis, point toward an intrinsic renal pathology, most notably nephritic syndrome or acute/chronic glomerulonephritis. To understand her condition, it is crucial to analyze her symptoms and laboratory data in detail.

Diagnosis of Angela’s Disorder

Based on her symptoms and lab results, Angela is most likely suffering from glomerulonephritis, an inflammatory disorder affecting the glomeruli of the kidneys. The red-brown urine suggests hematuria caused by glomerular injury, leading to the leakage of blood components into the urine. Her decreased GFR (40 mL/min) and elevated serum creatinine indicate impaired renal filtration, aligning with glomerular inflammation or damage. The low serum sodium (hyponatremia), high serum potassium (hyperkalemia), low hematocrit (anemia), and reduced urine output further support a diagnosis of renal impairment consistent with nephritic syndrome.

Potential Causes of the Disorder

Glomerulonephritis can be triggered by immune-mediated processes, infections (such as post-streptococcal glomerulonephritis), systemic autoimmune diseases (like lupus erythematosus), or other inflammatory states. In Angela's age group, post-infectious glomerulonephritis is common following streptococcal infections, which can cause immune complex deposition in the glomeruli, leading to leakage of blood and proteins, edema, and impaired kidney function. Other causes include vasculitis or membranoproliferative glomerulonephritis. Given her symptoms’ progression over months, a chronic inflammatory response or an autoimmune process could be involved.

Definitions of Hyponatremia and Hyperkalemia

Hyponatremia is a condition characterized by serum sodium levels falling below 135 mEq/L. It often results from excess water retention relative to sodium, commonly seen in conditions like congestive heart failure, SIADH (syndrome of inappropriate antidiuretic hormone secretion), or renal failure. Symptoms include nausea, headache, confusion, and in severe cases, seizures.

Hyperkalemia refers to elevated serum potassium levels above 5.0 mEq/L. It can result from impaired renal excretion, cellular breakdown, or shifts of potassium from intracellular to extracellular compartments. Clinical manifestations include muscle weakness, arrhythmias, and cardiac arrest if severe.

Causes of Hyponatremia and Hyperkalemia in Angela

In Angela’s case, impaired renal function reduces sodium reabsorption and potassium excretion. The damaged glomeruli and reduced GFR hinder the kidneys’ ability to regulate electrolytes, leading to dilutional hyponatremia and hyperkalemia. Specifically, the loss of sodium via damaged glomeruli may result in hyponatremia, while potassium retention due to decreased renal excretion causes hyperkalemia. Additionally, neurohormonal activation in kidney failure, including increased vasopressin, can exacerbate sodium imbalance.

Blood in Urine: Hematuria

The presence of blood in Angela’s urine, evident as red to brown coloration, indicates hematuria. This results from damage to the glomerular basement membrane or capillaries, allowing erythrocytes to leak into the urinary filtrate. In glomerulonephritis, immune complex deposition and inflammation compromise the integrity of glomerular filtration barriers, causing bleeding into the urine.

Renal Function Tests Compared to Normal

Angela’s GFR of 40 mL/min is significantly below the normal range of approximately 100-120 mL/min, indicating moderate to severe reduction in renal filtration capacity. Her serum creatinine (2.5 mg/dL) and BUN (24.0 mg/dL) are elevated, reflecting impaired excretory function. Her renal blood flow (RBF) of 280 mL/min is decreased from the normal (~600 mL/min), further confirming compromised renal perfusion. These findings collectively suggest acute or chronic renal injury and diminished renal clearance, characteristic of glomerular inflammation.

Cause of Swollen Feeling

The swelling experienced by Angela, also known as edema, stems from disrupted kidney function leading to fluid retention. The inflammation of glomeruli causes leakage of plasma proteins like albumin into the urine, reducing plasma oncotic pressure and resulting in generalized edema. Additionally, impaired sodium handling by the kidneys causes extracellular fluid accumulation, worsening swelling. The combination of low serum albumin, increased capillary permeability, and sodium retention contributes to her swollen sensation.

Conclusion

Angela’s clinical presentation and laboratory findings point toward a diagnosis of glomerulonephritis, likely of an immune-mediated origin. The renal impairment manifests with decreased GFR, electrolyte disturbances (hyponatremia and hyperkalemia), hematuria, and fluid retention resulting in swelling. Understanding the pathophysiology underlying her condition is essential for targeted management, which includes addressing the inflammatory process, correcting electrolyte imbalances, and supporting renal function. Early intervention is vital to prevent progression to end-stage renal disease and improve her prognosis.

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