Stage II, the tumor extends beyond the kidney but is completely resected. Stage II would be a tumor that has grown outside the kidney to some degree, such as into surrounding fatty tissue. Usually, the tumor would be completely removable by surgery, and regional lymph nodes are negative. About 20% of all Wilms tumors are at this stage.

Option A: This is not included in the staging of Wilms tumor. Imaging is particularly important in surgical planning. Surgical risk factors include larger tumor size, contralateral tumor extension, and displacement of the great vessels which typically result in longer surgical times, increased blood loss, and higher complication rates.
Option B: This described stage I: the tumor is limited to the kidney and completely resected. Stage I indicates the tumor was completely contained within the kidney without any breaks or spillage outside the renal capsule and no vascular invasion. This stage accounts for 40% to 45% of all Wilms tumors.
Option D: This described stage IV, hematogenous metastasis has occurred with spread beyond the abdomen. Stage IV tumors are those that have spread through the vascular system to distant organs such as the lungs, liver, brain, or bones, or to distant lymph nodes. These account for about 10% of all Wilms tumors.

Acute glomerulonephritis is characterized by high urine specific gravity related to oliguria as well as dark “tea-colored” urine caused by large amounts of red blood cells. As the glomerular filtration rate (GFR) is decreased, symptoms like edema and hypertension occur, majorly due to the subsequent salt and water retention caused by the activation of the renin-angiotensin-aldosterone system.

Option A: Glomerulonephritis and pyelonephritis cause a decreased urine volume and low specific gravity. In these diseases, damage to the kidney’s tubules affects the ability of the kidney to reabsorb water. As a result, the urine remains dilute.
Option B: About half of the people with acute glomerulonephritis have no symptoms. If symptoms do occur, the first to appear are tissue swelling (edema) due to fluid retention, low urine volume, and production of urine that is dark because it contains blood.
Option C: When kidneys are failing, the increased concentration and accumulation of substances in urine lead to a darker color which may be brown, red or purple. The color change is due to abnormal protein or sugar, high levels of red and white blood cells, and high numbers of tube-shaped particles called cellular casts.
Option D: There is periorbital edema, but generalized edema is seen in nephrotic syndrome, not acute glomerulonephritis. Edema may first appear as puffiness of the face and eyelids but later is prominent in the legs. This is reported in approximately 85% of pediatric patients; edema may be mild (involving only the face) to severe, bordering on a nephrotic appearance.
Option E: Patients often have a normal physical examination and blood pressure; most frequently, however, patients present with a combination of edema, hypertension, and oliguria. The physician should look for signs of fluid overload, like periorbital and/or pedal edema.

Acute glomerulonephritis is most commonly caused by the immune response to a prior upper respiratory infection with group A Streptococcus. PSGN most commonly presents in children 1 to 2 weeks after a streptococcal throat infection, or within 6 weeks following a streptococcal skin infection. Group A Streptococcus (GAS) has been subtyped depending on the surface M protein and opacity factor, which are known to be nephrogenic and can cause PSGN.

Option A: Glomerulonephritis is not a congenital condition. Nephrogenic streptococci infection precedes PSGN, which initially affects skin or oropharynx. More recently, PSGN is associated with skin infections (impetigo) more frequently than throat infections (pharyngitis).
Option C: Glomerular lesions in acute GN are the result of glomerular deposition or in situ formation of immune complexes. Poor hygiene, overcrowding, and low socioeconomic status are important risk factors for streptococci outbreaks, and this explains the higher incidence of PSGN in impoverished countries. Genetic factors are expected to predispose to the condition since almost 40% of patients with PSGN gave a positive family history. There is no specific gene found to cause PSGN.
Option D: Nephrotic syndrome is the combination of nephrotic-range proteinuria with a low serum albumin level and edema. It is caused by increased permeability through the damaged basement membrane in the renal glomerulus, especially infectious or thrombo-embolic. It is the result of an abnormality of glomerular permeability that may be primary with a disease-specific to the kidneys or secondary to congenital infections, diabetes, systemic lupus erythematosus, neoplasia, or certain drug use.

A hydrocele is a collection of fluid in the scrotum that results from a patent tunica vaginalis. Illumination of the scrotum with a pocket light demonstrates the clear fluid. In most cases the fluid reabsorbed within the first few months of life and no treatment is necessary.

Option A: Congenital hydrocele tends to be intermittent as it usually reduces when lying flat due to drainage of hydrocele fluid into the peritoneum. However, applying pressure on the congenital hydrocele does not reduce it. At birth, around 80-90% of term male infants possess a patent processus vaginalis. This figure declines steadily to settle at approximately 25-40% at two years of age.
Option B: Surgery is the treatment of choice for hydrocele, and it is warranted when hydrocele becomes complicated or symptomatic. For congenital hydroceles, herniotomy is performed, provided they do not resolve spontaneously. On the other hand, acquired hydroceles subside when the primary underlying condition resolves.
Option D: Placing the infant in a supine position would have no effect. The majority of patients with hydrocele present with the complaint of painless scrotal swelling rendering the testes impalpable with positive transillumination and fluctuation. The examiner should look at this swelling in both the supine and upright positions.

Patients with peripheral vascular disease often sustain nerve damage as a result of inadequate tissue perfusion. Intermittent claudication results when blood flow distal to the occlusion is sufficiently compromised, resulting in fixed oxygen delivery that is unable to match oxygen demand. The most severe form of PAD is critical limb ischemia, which is defined as limb pain at rest or impending limb loss.

Option B: Fluid overload is not characteristic of PVD. Atherosclerotic plaque builds up slowly over decades within the wall of the vessel. Plaque accumulation results in vascular stenosis and frequent vascular dilation to maximize end-organ perfusion. Once the vessel dilation capacity is maximized, the plaque continues to accumulate, which further compromises the lumen occasionally, leading to critical narrowing of the artery.
Option C: There is nothing to indicate psychiatric disturbance in the patient. The overall prognosis of patients with peripheral vascular disease must take into account patient risk factors, cardiovascular health, and disease severity. In terms of limb health at 5 years, nearly 80% of patients will have stable claudication symptoms. Only 1% to 2% of patients will progress to critical limb ischemia in 5 years. Twenty to 30% of patients with PAD will die within 5 years, with 75% of those deaths attributed to cardiovascular causes.
Option D: Skin changes in PVD are secondary to decreased tissue perfusion rather than primary inflammation. Examination of the limbs should involve assessment for pulselessness, pallor, muscular atrophy, cool or cyanotic skin, or pain with palpation. Lower extremity ulcers may be arterial, venous, neuropathic, or a combination of two or more. Ulcers secondary to arterial insufficiency are tender and typically have ragged borders with a dry base and pale or necrotic centers.