NAGAMATSU INCISION
DESCRIPTION A dorsolumbar incision is made over either the 11th or 12th rib, which is resected. After rib removal, the diaphragm and pleura are retracted superiorly, and the kidney and the adrenal may be exposed.
REFERENCE
Montague DK. Surgical incisions. In: Novick AC, Streem SB, Pontes JE, eds. Stewart’s Operative Urology. Baltimore, MD: Williams & Wilkins; 1989:15–40.
NATIONAL COMPREHENSIVE CANCER NETWORK (NCCN) GUIDELINES
DESCRIPTION The NCCN is a nonprofit alliance of NCI-designated Comprehensive Cancer Centers devoted to improving care for cancer patients. This includes the development of treatment guidelines for most cancers, including GU cancers such as prostate, bladder, kidney, and testes as well as screening guidelines. Patient friendly information is also available. Useful treatment algorithms are available on their site or as an app for mobile devices. Registration (no charge) is required. (See also Section II: “Prostate Cancer Screening Guidelines.”)
REFERENCE
Online at www.nccn.org.
NATIONAL INSTITUTES OF HEALTH (NIH) CHRONIC PROSTATITIS SYMPTOM INDEX (CPSI)
DESCRIPTION The CPSI is a validated and reproducible measure of outcomes for men with prostatitis. With 9 questions, it captures the 3 domains of the prostatitis experience: Pain, urinary function, and quality of life. While not a diagnostic aid, it is useful for both research studies and clinical practice, in initially assessing patients, subsequently following their progress, and providing specific treatment. (See Section VII.)
REFERENCE
Litwin MS, McNaughton-Collins M, Fowler FJ Jr, et al. The National Institutes of Health chronic prostatitis symptom index: Development and validation of a new outcome measure. J Urol. 1999;162:369–375.
NECROSPERMIA
DESCRIPTION A condition in which the sperm are both nonmotile and nonviable. The etiology of this condition is variable.
REFERENCE
Chavez-Badiola A, Drakeley AJ, Finney V, et al. Necrospermia, antisperm antibodies, and vasectomy. Fertil Steril. 2008;89(3):723.e5–e7.
NELSON SYNDROME
DESCRIPTION The development of pituitary tumors (usually a chromophobe adenoma) seen in 10–20% of patients originally treated with bilateral adrenalectomy for Cushing disease. Believed to be caused by a lack of hypothalamic/pituitary feedback and resultant high levels of ACTH and related compounds, patients must be followed with ACTH levels and imaging of the sella turcica. Patients usually present 1–4 yr after bilateral adrenalectomy. Common symptoms include visual deficits (57%), hyperpigmentation, and headaches, however most patients are diagnosed based on screening labs and imaging. ACTH levels above 200 ng/L and evidence of pituitary mass enlargement on MRI are diagnostic.
TREATMENT
• Surgical excision
• Radiation therapy
• Prophylactic pituitary radiotherapy (shown to reduce the incidence of Nelson syndrome by 50%)
REFERENCE
Banasiak MJ, Malek AR. Nelson syndrome: comprehensive review of pathophysiology, diagnosis, and management. Neurosurg Focus. 2007;23(3):E13.
NEPHRITIS, RADIATION
DESCRIPTION Renal dysfunction occurs if ≥23 Gy of radiation therapy is administered to both kidneys during a period of ≤5 wk. Histologic exam shows hyalinized glomeruli, atrophic tubules, interstitial fibrosis, and hyalinization of the media of renal arterioles. Radiation-induced renal ischemia causes tubulointerstitial damage, which may take months to manifest. Acute radiation nephritis presents with rapidly progressing azotemia, moderate to malignant hypertension, anemia, and proteinuria. More than 50% of patients progress to chronic renal failure. Malignant hypertension may follow unilateral radiation and resolve with nephrectomy. This entity has essentially vanished due to refinement in radiation therapy techniques.
REFERENCE
Kelly CJ, Neilson EG. Tubulointerstitial diseases. In: Brenner BM, ed. The Kidney. 5th ed. Philadelphia, PA: Saunders; 1996:1655–1679.
NEPHROCALCINOSIS, NEONATAL
DESCRIPTION Nephrocalcinosis with or without nephrolithiasis are commonly observed in both term and premature infants who have had difficult neonatal courses. Neonates with prolonged illness are at particular risk, especially those who still require oxygen at 28 days. While multifactorial, such as high calcium and phosphorous intake, loop diuretics appear to be the major cause in this group of patients. Loop diuretics (furosemide most commonly used) predispose to nephrocalcinosis by increasing urinary calcium excretion. Other factors such as immature renal function and physiologic hypercalciuria that occurs between 32 and 40 weeks of gestation contribute.
Nephrocalcinosis in infants with a birth weight <1,500 g may be as high as 64% and may be independent of diuretic use. In infants born <32 wk gestation, 27% had nephrocalcinosis with 70% having been treated with a loop diuretic. Other causes of neonatal nephrocalcinosis include William syndrome (supravalvular aortic stenosis and hypercalcemia), neonatal primary hyperparathyroidism and distal (type 1) renal tubular acidosis. The loop diuretic-induced hypercalciuria can be diminished and radiologic appearance of renal calcifications diminished by administrating a thiazide diuretic in place of or alternating with a loop diuretic. The long-term impact of nephrocalcinosis on renal outcome is unclear because data are limited and inconsistent. Long-term follow-up is recommended.
REFERENCE
Smith J, Stapleton FB. Nephrocalcinosis in neonates. www.UpToDate.com; Wolters Kluwer, Accessed March 29, 2014.
NEPHROGENIC ADENOMA (NA) AND METAPLASIA
DESCRIPTION A rare lesion occurring in the urinary tract that was once thought to be a metaplastic reaction to chronic irritation and has now been shown to originate from exfoliated and implanted renal epithelial cells. It is named for its histologic similarity to renal tubules and can cause hematuria, dysuria, and urinary frequency. On cystoscopy nephrogenic adenoma can appear papillary, nodular, or sessile and is very friable. It is typically unifocal. It is considered a benign lesion, however malignant transformation has been reported and therefore requires complete resection and long-term follow-up due to recurrence rates from 0.5–80% (Image 
).
REFERENCE
Alexiev BA, LeVea CM. Nephrogenic adenoma of the urinary tract: A review. Int J Surg Pathol. 2012;20(2):123–131.
NEPHROGENIC SYNDROME OF INAPPROPRIATE ANTIDIURESIS
DESCRIPTION A clinical disorder of water balance resulting in an inability to excrete a free water load. Clinically patients appear similar to those with SIADH, however they have low serum levels of circulating vasopressin. Activating mutations of the V2R (vasopressin type 2 receptor) have been identified as a cause of this chronic condition. Treatment of this condition includes free water restriction and osmotic diuresis with urea. Targeted treatment with compounds that might inhibit V2R are under investigation.
REFERENCE
Feldman BJ, Rosenthal SM, Vargas GA, et al. Nephrogenic syndrome of inappropriate antidiuresis. N Engl J Med. 20005;352:1885–1890.
NEPHROGENIC SYSTEMIC FIBROSIS/FIBROSING DERMATOPATHY (NSF/NFD)
DESCRIPTION NSF is a scleroderma-like skin disease that affects patients with renal insufficiency. There is a strong association between the development of NSF and exposure to gadolinium contrast agents used in performing MRI in patients with advanced kidney disease. The skin lesions begin as patches, plaques, or papules, then coalesce to form a woody skin appearance. The skin thickening can limit joint motion. There is no known effective treatment. (See also Section I: “Contrast Allergy and Reactions.”)
REFERENCE
Kurtkoti J, Snow T, Hiremagalur B. Gadolinium and nephrogenic systemic fibrosis: Association or causation. Nephrology. 2008;13:235–241.
NEPHROMETRY SCORING SYSTEMS (PADUA, C-INDEX, RENAL)
DESCRIPTION Nephrometry is an attempt to create a common classification system to describe renal masses based on anatomical characteristics. 3 prominent scoring systems have emerged. PADUA (Preoperative aspects and dimensions used for anatomic classification), C-Index (centrality index), and RENAL (radius, exophytic/endophytic, nearness, anterior/posterior, location) all attempt to score and categorize renal tumors in an attempt to predict complexity of nephron-sparing surgery and surgical outcomes of these lesions.
REFERENCE
Okhunov Z, Rais-Bahrami S, George AK, et al. The comparison of three renal tumor scoring systems: C-index, P.A.D.U.A., and R.E.N.A.L. nephrometry scores. J Endourol. 2011;25(12):1921–1924.
NEPHRONOPHTHISIS (JUVENILE, INFANTILE, AND ADOLESCENT)
DESCRIPTION A group of 4 diseases, known as the juvenile nephronophthisis–renal medullary cystic disease complex, that result in ESRD. Nephronophthisis is the most common cause of tubointerstitial nephropathy in children, and is inherited in an autosomal recessive pattern mapped to chromosome 2. 3 subtypes of nephronophthisis exist, based on the age of onset of ESRD. Juvenile nephronophthisis is the most common (1 in 50,000 births), with a median onset of 13 yr; infantile nephronophthisis usually causes ESRD by 5 yr; and adolescent nephronophthisis has a mean onset of 19 yr. The disease presents as failure to thrive, azotemia, polyuria, and polydipsia. Hypertension is less common. Microscopically, it resembles an interstitial nephritis with cysts. US reveals muddling of corticomedullary junction and small reniform kidneys with cysts found at the corticomedullary junction. Retinitis pigmentosa hepatic fibrosis and Bardet–Biedl syndrome are associated. Renal replacement therapy, as needed, is the treatment of choice. Extrarenal involvement is described and can involve the retina, liver, and brain. (See also Section I: “Medullary Cystic Kidney Disease.”)
REFERENCE
Saunier S, Salomon R, Antignac C. Nephronophthisis. Curr Opin Gen Dev. 2005;15:324–331.
NEPHROPATHY, ANALGESIC
DESCRIPTION A chronic interstitial nephritis seen in patients who consume large quantities of analgesics over many years. They usually suffer from chronic headaches or low back pain and have consumed a mixture of analgesics, including acetaminophen, aspirin, and NSAIDs. Their chronic use leads to recurrent papillary necrosis with impaired concentrating ability, sterile pyuria, and renal insufficiency. Removal of phenacetin from OTC pain medications has dramatically reduced the incidence of this condition. During periods of acute necrosis, patients may have flank pain, pyuria, hematuria, and acute ureteral obstruction from passage of sloughed, necrotic papillary tissue. IVP shows the ring sign, which refers to the contrast agent surrounding sloughed papilla, although the current use of IVP is limited due to contrast load. Renal US shows small kidneys, with irregular thinning of the renal cortex. Renal biopsy shows interstitial infiltrates and fibrosis. Noncontrast CT shows bilateral reduced renal size, bumpy renal contours, and papillary calcifications (ie, small, indented, and calcified kidneys). The mechanism of injury is believed to be a combination of injury from the production of toxic metabolites and medullary ischemia. These patients are at increased risk of developing TCC of the urinary tract. Cessation of drug use can lead to stabilization of renal function.
REFERENCE
Mihatsch MJ, Khanlari B, Brunner FP. Obituary to analgesic nephropathy—an autopsy study. Nephrol Dial Transplant. 2006;21(11):3139–3145.
NEPHROPATHY, ISCHEMIC
DESCRIPTION Ischemic nephropathy is described as a deterioration of renal function due to a reduction in renal blood flow, commonly caused by atherosclerotic renovascular disease or renal artery stenosis. The disease progresses with worsening renal failure and decreased overall survival. It can present as hypertension (HTN) with unexplained renal insufficiency, worsening azotemia with HTN, azotemia in the setting of coronary artery disease or peripheral vascular disease, ACE inhibitor-induced ARF, or flash pulmonary edema. Numerous tests are used to define the presence, size, and function of the kidneys, as well as to establish the presence of a vascular lesion and its clinical significance, including CT or MR angiography, conventional angiography, Doppler US, ACE-I renography or renal vein renin measurements. Controversy still exists on the appropriate management of renal artery stenosis. Options include medical therapy, percutaneous transluminal angioplasty with or without stent placement, as well as surgical revascularization or nephrectomy. (See also Section I: “Renal Artery Stenosis/Renovascular Hypertension.”)
REFERENCE
Chonchol M, Linas S. Diagnosis and management of ischemic nephropathy. Clin J Am Soc Nephrol. 2006;1:172–181.
NEPHROPATHY, MEMBRANOUS
DESCRIPTION Renal disease that manifests with nephrotic syndrome. Affecting mainly middle-aged adults, it can progress to either spontaneous remission or ESRD. It is the most common cause of nephrotic syndrome in nondiabetic adults. Proteinuria with microscopic hematuria is often present; massive proteinuria, hypertension, and impaired renal function on presentation, and male gender, are all poor prognostic factors. Believed to be related to in situ formation of immune complexes, it is most commonly idiopathic, but may be secondary to diseases (malignancy, infection, systemic lupus erythematosus [SLE]) or drug use (gold, penicillamine). Immunofluorescence often reveals deposits of IgG and complement. Treatment is based on the risk of progression associated with proteinuria (low risk <4 g/protein/d; moderate 4–8 g/protein/d; high risk >8 g/protein/d, lasting >3 mo or associated with a reduced creatinine clearance). Low-risk patients are at high likelihood of spontaneous remission and are treated with nonimmunosuppressive therapy, including ACE inhibitors or angiotensin II receptor blockers. In high-risk disease, cyclophosphamide and chlorambucil, both given with glucocorticoids, are effective in inducing remission of proteinuria and preventing progression to ESRD. Other agents reported include cyclosporine and tacrolimus (plus low-dose prednisone 10 mg/d max). (See also Section I: “Nephrotic Syndrome.”)
REFERENCE
Glassock RJ. Diagnosis and natural course of membranous nephropathy. Semin Nephrol. 2003;23(4):324–332.
NEPHROPATHY, MINIMAL CHANGE
DESCRIPTION A common cause of nephrotic syndrome, most often affecting children but can account for up to 15% of adult nephrotic syndrome. Sometimes called minimal change disease, this condition manifests as nephrotic syndrome, with massive proteinuria and anasarca without hypertension. RBCs in the urine are a common finding; histologic evaluation shows essentially no changes on light microscopy. Electron microscopy shows epithelial foot process fusion. The pathogenesis is unknown, but T-cell dysfunction is theorized. The nephropathy can be primary or secondary to medications, neoplasm, infection, allergy, or other renal glomerular diseases; it frequently undergoes spontaneous remission, is responsive to corticosteroid therapy, and rarely progresses to chronic renal failure. (See also Section I: “Nephrotic Syndrome.”)
REFERENCE
Waldman M, Crew RJ, Valeri A, et al. Adult minimal-change disease: Clinical characteristics, treatment, and outcomes. Clin J Am Soc Nephrol. 2007;2(3):445–453.
NEPHROPATHY, OBSTRUCTIVE
DESCRIPTION Obstructive nephropathy occurs when renal deterioration is due to obstruction of the urinary system. The point of obstruction can be in the upper or lower urinary tract. Congenital, inflammatory, neoplastic, and anatomic etiologies of urinary obstruction are all common. Obstruction of the outflow from the kidney results in several changes that lead to renal fibrosis. The tubular injury in obstructive nephropathy is caused initially by the increased intratubular pressure and later by atrophy induced by reduced perfusion, inflammation, and ischemia. The recovery of renal function after relief of the obstruction is determined by the duration of the obstruction, baseline renal function, patient age, and degree of obstruction. With total obstruction of the ureter, relatively complete recovery of GFR can be achieved within 1 wk, whereas after 12 wk, little or no recovery is seen. (See also Section I: “Hydronephrosis/Hydroureteronephrosis [Dilated Ureter/Renal Pelvis], Adult.”)
REFERENCE
Better OS, Arieff AI, Massry SG, et al. Studies on renal function after relief of complete unilateral ureteral obstruction of three months duration in man. Am J Med. 1973;54(2):234–240.
NEPHROPATHY, URATE (URATE NEPHROPATHY)
DESCRIPTION A disorder in which an abrupt deterioration in renal function occurs due to the renal tubular deposition of urate and uric acid crystals. Chronic renal injury from uric acid deposition is most often associated with gout and is uncommon today. 2 forms are recognized, acute and chronic. Acute urate nephropathy occurs almost exclusively in the setting of malignancies, such as leukemias and lymphomas, with rapid cell turnover leading to increased purine metabolism and loss of nucleotides in the plasma. This is further enhanced by added acceleration of cell lysis, which occurs with chemotherapy and radiation used in these patients, producing the so-called tumor lysis syndrome. Nucleotides are converted to urate by xanthine oxidase, resulting in hyperuricemia with levels of 25–90 mg/dL at the time of onset of renal dysfunction. Diagnosis requires the appropriate clinical setting of increased cell lysis (usually with chemotherapy), oliguria, marked hyperuricemia, and hyperuricosuria. A urinary uric acid-to-creatinine ratio >1 distinguishes this from other catabolic states with elevated serum urate levels and renal failure, such as trauma with rhabdomyolysis. (See also Section I: “Urolithiasis, Uric Acid”; Section II: “Gout, Urologic Considerations,” “Hyperuricosuria,” and Tumor Lysis Syndrome [TLS].”)
TREATMENT
• Prevention is the key, using xanthine oxidase inhibition with allopurinol and alkaline diuresis prior to initiation of chemotherapy.
• Alkalinization of urine in the acute tumor lysis syndrome is not possible in the setting of brisk diuresis.
• Rasburicase (Elitek) is recombinant urate oxidase that converts uric acid to water-soluble allantoin.
• Occasionally, dialysis is required to correct azotemia and reduce urate levels.
REFERENCE
Conger JD. Acute uric acid nephropathy. Med Clin North Am 1990;74:859–871.
NEPHROPTOSIS
DESCRIPTION Nephroptosis, also referred to as floating kidney or renal ptosis, is a condition in which the kidney drops into the pelvis when the patient stands up. It tends to be more common in women and is thought to be caused by a lack of perirenal fat. Patients are usually asymptomatic but colicky type pain can be attributed to this conditions, similar to a Dietl crisis. The pain is classically relieved by lying down. Imaging can demonstrate the renal descent and aid in diagnosis. Conservative management had been the mainstay of treatment, although laparoscopic nephropexy is now recommended for symptomatic patients. (See also Section II: “Dietl Crisis.”)
REFERENCE
Barber NJ, Thompson PM. Nephroptosis and nephropexy-hung up on the past? Eur Urology. 2004;46:428–433.
NESBIT CHORDEE REPAIR
DESCRIPTION A surgical procedure in which ≥1 vertical ellipses are removed from the Tunica Albuginea on the longer convex side, and the ellipses are closed transversely, which results in shortening of the longer side to correct the penile curvature.
REFERENCE
Montague DK. Correction of chordee. In: Novick AC, Streem SB, Pontes JE, eds. Stewart’s Operative Urology. Baltimore, MD: Williams & Wilkins; 1989:822–825.
NEUROENDOCRINE TUMORS, GENITOURINARY
DESCRIPTION A group of tumors that share a characteristic morphology, often being composed of clusters and trabecular sheets of round blue cells, granular chromatin, and an attenuated rim of poorly demarcated cytoplasm. Neuroendocrine tumors include carcinoids, small (oat) cell carcinomas, medullary carcinoma of the thyroid, Merkel cell tumor, cutaneous neuroendocrine carcinoma, pancreatic islet cell tumors, and pheochromocytoma. Small (oat) cell carcinomas have been described most often in the prostate and bladder. Prostate cancer with neuroendocrine differentiation is considered a variant of Gleason 5 adenocarcinoma of the prostate. Undifferentiated carcinomas of the urinary bladder and prostate should be analyzed not only by means of hematoxylin and eosin but also by immunohistochemical staining for chromogranin A (Chr A) and synaptophysin (SNP), to demonstrate a neuroendocrine origin. Because the prognosis of small cell neuroendocrine cancers is very poor, aggressive multimodal therapy is often employed. (See also Section I: “Pheochromocytoma”; Section II: “Multiple Endocrine Neoplasia [MEN I, MEN II]”; “Prostate Cancer, Small Cell [Neuroendocrine].”)
REFERENCE
Helpap B. Morphology and therapeutic strategies for neuroendocrine tumors of the genitourinary tract. Cancer. 2002;95(7):1415–1420.
NEUROFIBROMATOSIS, UROLOGIC CONSIDERATIONS
DESCRIPTION A hereditary disorder characterized by cafe-au-lait spots, cutaneous fibromas, and neurofibromas; it is associated with renovascular lesions and pheochromocytomas. Vascular lesions are characterized by endothelial proliferation, with or without aneurysmal formation and cellular nodules in the vessel walls. The aorta is frequently involved, and the renal arteries may demonstrate long areas of stenosis that are generally best treated with revascularization rather than angioplasty. In addition, a 30-fold increase in the incidence of neurofibromatosis in patients with Wilms tumor has been reported.
REFERENCE
Saborio P, Scheinman J. Genetic renal disease. Curr Opin Pediat. 1998;10:174–183.
NEUROGENIC DETRUSOR OVERACTIVITY (NDO)
DESCRIPTION NDO patients are a heterogeneous group with both storage and voiding dysfunction. The NDO symptoms include urinary frequency, urgency, and incontinence. Neurologic conditions associated with NDO include multiple sclerosis (MS), spinal cord injury (SCI) Parkinson disease, cerebral palsy, and myelomeningocele. Neurogenic bladder dysfunction is present in 80.8% of individuals with MS, 90% with myelodysplasia, virtually all SCI patients with persistent neurologic deficits and 70% of ambulatory SCI patients. NDO impacts quality of life and can also result in risk of UTI and upper urinary tract damage.
Anticholinergic therapies such as oxybutynin are primarily used for patients with DO and poor compliance. CIC may be best for those who have poor bladder emptying. Although not FDA-approved neuromodulation via sacral nerve stimulation is useful in patients who have failed anticholinergics. Intra-detrusor injection of onabotulinum toxin-A is FDA approved in the management of NDO in patients refractory or intolerant of anticholinergics. In selected individuals, a chronic indwelling catheter may be the best management therapy. Surgical intervention (bladder augmentation, urinary diversion, continent urinary diversion, and ileovesicostomy) may be indicated for protection of the upper urinary tract in high-risk patients or to achieve continence. (See also Section I: “Neurogenic Bladder, General Considerations.”)
REFERENCE
Cone E, Ellsworth P. Neurogenic detrusor overactivity: An update on management options. R I Med J. 2013, Available at www.rimed.org, Accessed March 29, 2014.
NEUROMODULATION, UROLOGIC CONSIDERATIONS
DESCRIPTION Neuromodulation involves the use of electrical current to alter physiologic properties. This technology has been applied to lower urinary tract voiding dysfunction for the past decade by stimulation of the sacral nerve roots. Sacral neuromodulation was approved for use in patients with overactive bladder refractory to medical and behavioral therapy by the FDA in 1997. A recent multi-institutional clinical trial shows success rates as high as 68% for urge urinary incontinence, 56% for urgency–frequency, and 71% with unobstructive urinary retention at 5 yr after implantation. Posterior tibial nerve stimulation is also being used. (See also Section II: “Posterior Tibial Nerve Stimulation: Urgent PC [PTNS].”)
REFERENCE
Hubsher CP, Jansen R, Riggs DR, et al. Sacral nerve stimulation for neuromodulation of the lower urinary tract: How I do it. Can J Urol. 2012;19(5):6480–6484.
NEVES–ZINCKE CLASSIFICATION
DESCRIPTION A largely historic classification system for describing the level of tumor thrombus associated with a renal mass. The categories are renal vein, ≤2 cm above the renal vein, infrahepatic >2 cm but below the intrahepatic vena cava, intrahepatic but below the diaphragm and atrial above the diaphragm. (See also Section I: “Renal Cell Carcinoma with Tumor Thrombus.”)
REFERENCE
Neves RJ, Zincke H. Surgical treatment of renal cancer with vena cava extension. BJU. 1987;59(5):390–395.
NMP-22 TESTING
DESCRIPTION NMP-22 has been found to serve as a urinary marker for TCC. The NMP-22 test (Matritech, Inc., Newton, MA) is a quantitative immunoassay that measures NMP-22. The addition of NMP-22 testing to cytology may increase the sensitivity for recurrence detection in patients with superficial transitional cell bladder cancer. Patients with positive NMP-22 findings developed significantly more recurrences compared with those with negative NMP-22 findings in several studies.
REFERENCE
Gupta NP, Sharma N, Kumar R. Nuclear matrix protein 22 as adjunct to urine cytology and cystoscopy in follow-up of superficial TCC of urinary bladder. Urology. 2009;73(3):592–596.
NOCTURNAL ERECTIONS, NORMAL AND ABNORMAL
DESCRIPTION Nocturnal erections occur at night during REM sleep. The number of erections peak during puberty. Various criteria exist for what is considered normal erectile activity at night, but normal is usually 4–5 erectile episodes per night with a mean duration >30 min and an increase in circumference of >3 cm at the base and >2 cm at the tip, as well as maximal rigidity above 70% at both base and tip. (See also Section II: “Nocturnal Penile Tumescence Testing.”)
REFERENCE
Lue TF, Broderick GA. Evaluation and nonsurgical management of erectile dysfunction and premature ejaculation. In: Wein AJ, Kavoussi LR, Novick AC, et al., eds. Campbell-Walsh Urology. 9th ed. Philadelphia, PA: Saunders Elsevier; 2007:765.
NOCTURNAL PENILE TUMESCENCE (NPT) TESTING
DESCRIPTION NPT refers to a recurring cycle of penile erections associated with rapid eye movement sleep. The primary goal of NPT testing is to distinguish between psychogenic and organic causes of impotence. Nocturnal monitoring devices measure the number of erectile episodes, maximal penile rigidity, tumescence, and duration of erections. This testing assumes that the mechanism for nocturnal erections is the same as that for erotically induced erections. (See also Section II: “Nocturnal Erections, Normal and Abnormal.”)
REFERENCE
Greenstein A, Mabjeesh NJ, Sofer M, et al. Are consecutive nightly recordings required for valid evaluation of sleep-associated erections? Int J Impot Res. 2007;19(2):196–199.
NOCTURNAL POLYURIA (NP)
DESCRIPTION NP is a condition in which the rate of urine output is excessive only at night, and total 24-hr output is within normal limits. NP is defined as the production of >1/3 of total 24-hr urine output between midnight and 8 AM (normal physiologic response is reduced urine output at night). A voiding diary (frequency volume chart or FVC) that records time and volume of each void over a 24-hr period for 7 days establishes if the patient is polyuric or nonpolyuric. True polyuria is present throughout the 24-hr period, whereas NP is confined to elevated night-time output. Altered sleep patterns caused by frequent trips to the bathroom can cause problems staying alert at work, major depression, and hypertension. Although traditional therapies in men have been directed toward medical or surgical treatment, NP does not respond well to these standard interventions. (See also Section II: “Polyuria and Voiding Diary [Frequency Volume Chart, FVC].”)
TREATMENT
• Lifestyle changes: Limiting fluids in the late afternoon and evening, such as coffee, soft drinks, or tea.
• Taking diuretics early in the day.
• Desmopressin mimics the action of vasopressin in reducing nocturnal urine production.
REFERENCE
Kujubu DA, Aboseif SR. An overview of nocturia and the syndrome of nocturnal polyuria in the elderly. Nat Clin Pract Nephrol. 2008;4(8):426–435.
NOMOGRAMS, UROLOGIC
DESCRIPTION Nomograms are mathematical tools that allow for the prediction of various outcomes. Validated nomograms have been developed for all major urologic cancers, as well as for some benign urologic diseases. Useful online prediction tools are available on several sites including Memorial Sloan Kettering Cancer Center (www.mskcc.org/mskcc/html/5794.cfm) for prostate, bladder, and kidney cancer. SWOP is sponsored by the Prostate Cancer Research Foundation, Rotterdam (www.prostatecancer-riskcalculator.com/). It is an online multi-step Prostate Cancer Risk Calculator and assesses a man’s prostate cancer risk and helps to avoid unnecessary biopsy.
REFERENCE
Kattan MW, Scardino PT. Evidence for the usefulness of nomograms. Nat Clin Pract Urol. 2007;4(12):638–639.
NONARTERITIC ANTERIOR ISCHEMIC OPTIC NEUROPATHY (NAION)
DESCRIPTION NAION describes the acute, painless loss of vision in 1 eye associated with optic disc edema (crowded optic disk). It is a common cause of acute optic neuropathy in adults. Associations have been found between NAION and the phosphodiesterase inhibitors sildenafil, vardenafil, and others. The mechanism and exact nature of this association are still under investigation.
REFERENCE
Seftel AD, Miner MM, Kloner RA, et al. Office evaluation of male sexual dysfunction. Urol Clin N Am. 2007;34:463–482.
NONSACRAL NEUROMODULATION
DESCRIPTION Neuromodulation involves the use of electrical current to alter physiologic properties. This technology has been applied to lower urinary tract voiding dysfunction for the past decade by stimulation of the sacral nerve roots. There has been recent interest into stimulation of more distal branches of the sacral nerve roots as well, including the pudendal, dorsal genital, and posterior tibial nerves. (See also Section II: “Neuromodulation, Urologic Considerations” and “Posterior Tibial Nerve Stimulation: Urgent PC [PTNS].”)
REFERENCE
Bennett RC, et al. Nonsacral neuromodulation. In: Goldman HB, Vasavada SP, eds. Female Urology: A Practical Clinical Guide. Totowa, NJ: Humana Press; 2007.
NOONAN SYNDROME
DESCRIPTION This autosomal dominant syndrome consists of multiple congenital anomalies, including characteristic facial features, short stature, and chest deformity. Over 1/2 of males with Noonan syndrome have unilateral or bilateral cryptorchidism. Females can have delayed sexual maturation, but normal development is expected. Renal anomalies occur in 10% of children. Because congenital cardiac anomalies are found in 1/2 of the patients, all patients with this syndrome should have cardiac evaluation and close follow-up. Growth hormone replacement may have value in treating short stature.
REFERENCE
Noonan JA. An update and review for the primary pediatrician. Pediatrics. 1997;33:549.
N-TELOPEPTIDE, URINARY (NTX)
DESCRIPTION NTX is a product of type I collagen breakdown that can be measured in the urine. Several studies suggest its utility as a marker for bone turnover in osteoporosis, and for response to treatment of bony metastasis and bisphosphonate therapy. Typical reference ranges are (bone collagen equivalent [BCE]): Normal adult male 21–83 nM BCE/mM creatinine; adult female premenopausal: 17–94 nM BCE/mM creatinine; postmenopausal 26–124 nM BCE/mM creatinine. A decrease of 30–40% from the NTX baseline after 3 mo of therapy is typical for treatment with bisphosphonate.
REFERENCE
Rubin CT, Rubin JE. Biology, physiology, and morphology of bone. In: Harris ED, Budd RC, Genovese MC, et al., eds. Kelley’s Textbook of Rheumatology. 7th ed. Philadelphia, PA: Saunders; 2005.
NUTCRACKER SYNDROME
DESCRIPTION This syndrome occurs secondary to compression of the left renal vein by the superior mesenteric artery and the aorta. Patients are usually young and previously healthy. Presentation classically is due to gross hematuria caused by left renal vein hypertension. Pelvic pain may be present. Various modalities, including nephrectomy, autotransplantation, renocaval reimplantation, and venolysis have been employed. Gore-Tex graft renal vein interposition and anterior nephropexy have been successful (Image ).
REFERENCE
Wang L, Yi L, Yang L, et al. Diagnosis and surgical treatment of nutcracker syndrome: A single-center experience. Urology. 2009;73(4):871–876.