George, a 26-year-old patient, presents to the Emergency Department (ED) with fever, chills, headache, stiff neck (nuchal rigidity), pain in the back, abdomen and extremities, as well as nausea and vomiting. George lives in a commune with many people in close quarters. He has been diagnosed with meningitis. What is meningitis? Which of the following would be most concerning regarding George's living situation and risk for meningitis? (Select all that apply, all. some or none)

A. Glomerulonephritis: This is an immune-mediated condition involving inflammation of the glomeruli and typically presents with proteinuria, hematuria, hypertension, and edema rather than urinary frequency, burning, or foul-smelling urine. The presence of E. coli and leukocytes does not support this diagnosis.

B. Kidney calculi: Kidney stones may present with flank pain, hematuria, and sometimes nausea or vomiting, but are not usually associated with urinary frequency, burning, or bacterial growth on urine culture. Randi’s symptoms point more toward an infectious etiology rather than a structural obstruction.

C. Lower UTI: cystitis (bladder infection) and possibly lower ureters: The burning, itching, frequent urination, and foul smell are classic signs of cystitis. The absence of flank pain and only a slightly elevated temperature further supports a lower tract infection rather than an upper one.

D. Upper UTI (pyelonephritis): Pyelonephritis typically presents with fever over 101°F, chills, nausea, vomiting, and significant costovertebral angle (CVA) tenderness or back/flank pain. Since Randi denies back pain and has only a mild temperature elevation, an upper UTI is unlikely.

A. Acute renal disease–acute glomerulonephritis: This leads to inflammation and damage of the glomerular basement membrane, impairing filtration and causing intrarenal injury. It often presents with hematuria, proteinuria, and hypertension.

B. Exposure to nephrotoxic drugs, heavy metals, and organic solvents: These substances damage renal tubules through direct toxicity or by causing crystal formation, leading to acute tubular necrosis. Common agents include aminoglycosides and contrast dyes.

C. Prolonged renal ischemia: Sustained low perfusion causes tubular cell death and sloughing, leading to obstruction and decreased GFR. It is often a progression from untreated prerenal AKI.

D. Liver failure: Liver dysfunction reduces renal perfusion and may cause hepatorenal syndrome, but this is classified as prerenal, not intrarenal, in origin. The kidneys are structurally intact but functionally impaired.