Introduction

Renal obstruction is one of the most commonly managed conditions by urologists, and the pathophysiology of this ailment lies at the intersection of urology and nephrology. In the acute setting, this situation can cause significant pain, places the patient at risk for severe sepsis if associated with infection, and when bilateral (or in a solitary kidney) can result in acute renal failure requiring dialysis. When it becomes chronic, tubular atrophy, inflammatory processes resulting in fibrosis, and an irreversible loss of nephrons and renal function will ultimately occur.

A comprehensive understanding of the disease process is critical for all urologists to appreciate. This chapter will outline the myriad causes of renal obstruction and focus most closely on those aspects of pathophysiology most relevant for the urologist. A brief overview of the management options will be discussed but a comprehensive discussion of these many options is beyond the purview of this chapter.

Normal Renal Physiology

For the purposes of understanding the pathophysiologic processes occurring with obstruction of the kidney, a brief overview of nephron function and physiology will be essential [1]. The functional unit of the kidney is the nephron, a single filtration unit that acts in concert with hundreds of thousands of other nephrons, varying in length and their exact architecture throughout the kidney. The nephron is composed of several parts (Fig. 12.1)—afferent and efferent blood supply, the glomerulus within Bowman’s capsule, the proximal convoluted tubule, the loop of Henle (thick descending limb, thin loop, the thick ascending limb) the distal convoluted tubule, and the collecting duct [1–3].

The glomerulus functions as a biological sieve, separating protein and blood cells from the fluid within Bowman’s capsule ; it is the site of filtration for the nephron. Blood passes first from the afferent arteriole and filters through the glomerulus into Bowman’s capsule where changes in pressure within the kidney (as a result of obstruction) will alter the hydrostatic forces facilitating this initial filtration step [4]. This filtration rate is expressed mathematically as the Glomerular Filtration Rate (GFR), where GFR = Kf(P _GC − P _T − π_GC). Kf: Glomerular filtration coefficient, P _GC: Glomerular capillary pressure, P _T: Tubular Pressure, and π _GC: oncotic pressure of the Glomerular capillary . The filtrate will pass through the aforementioned nephron segments, passing from the outer cortex, into the inner medulla and back repeatedly. Active and passive transport mechanisms ensure the exchange of ions and steep concentrations gradient occur—permitting excretion of excess water, urea, and unneeded ions and other solutes. After passing through each segment, the urine eventually exits the duct of Bellini to mix with urine within the calyx, infundibulum and eventually the renal pelvis [5].

A variety of solutes are transported back into the blood prior to leaving the nephron as urine as the fluid is traverses through the nephron. At the glomerulus, large molecules are initially filtered. The filtered solution is rich in glucose, sodium, chloride, potassium, and other ions. In the proximal convoluted tubule, approximately 60% of sodium, potassium, and calcium ions are resorbed along with 80% of phosphate, water, and bicarbonate molecules; nearly 100% of glucose is returned to the systemic circulation during this initial stage. A steep interstitial concentration gradient is produced, up to 1400 mOsm/kg, as the fluid descends down the thick limb of the loop of Henle into the papilla. Within this distal papillary interstitial space, the osmotic gradient is driven largely by urea [1]. This region of the nephron is notoriously poorly perfused and is often subject to ischemic insult during episodes of hypotension or obstructive processes.

Traveling through the distal papilla, the uriniferous fluid becomes increasingly hypotonic in comparison to the interstitium. It is here that solutes are transported out of the tubule and into the interstitium, where at the papillary tip the interstitium reaches the highest solute concentration. Ion exchange in the papilla maintains charge neutrality. If the organism becomes dehydrated, this will cause a shift in the generally water-impermeable collecting duct, facilitating reuptake of water through surface expression of aquaporins via antidiuretic hormone action. The steep concentration gradient makes water resorption thermodynamically favorable and helps to re-establish total body fluid homeostasis.

Etiologies, Pathogenesis and Prevalence

Urinary tract obstruction can occur at the level of the kidney, ureter, bladder, or the bladder outlet. At each of these locations, the etiology of the obstruction can be congenital or acquired (malignant or benign). The consequences vary depending if the obstruction is complete or partial and can range from an incidental finding to one which is painful, or from metabolic abnormalities to renal failure, and in severe cases can ultimately result in death. With each etiology, the consequences and permanence of the damage increase with the duration of the obstruction. In this section we will review some cases which may have relevance for the urologist in consideration of obstructive renal pathophysiology.

Bladder Outlet Obstructions

One of the most common causes of bilateral hydronephrosis are bladder outlet obstructions including those originating from benign prostatic hyperplasia, trauma, urethral stricture disease, vesicovaginal prolapse, and obstructing pelvic malignancies. Bladder outlet obstructions can be either intrinsic (benign prostatic hyperplasia or prostatic malignancy, urethral stricture or penile cancer, bladder neck contracture [de novo or post-operative]), or extrinsic (i.e. malignancies or mass effect from the colon, rectum, uterus, cervix, etc.).

Consider the case of a 33-year-old male who presented with acute urinary retention , low abdominal pain and bilateral flank pain (Fig. 12.2). On further evaluation he was found to have a bulbar urethral stricture after a distant straddle injury while riding a bicycle. A computerized tomography (CT) scan revealed bilateral hydroureteronephrosis along with a markedly distended bladder. The patient initially was managed with a suprapubic catheter for bladder decompression, and ultimately required a buccal mucosal graft urethroplasty to eliminate the urethral obstruction, shown in the preoperative retrograde urethrogram. In this case, the hydronephrosis was due to angulation of the ureterovesical junction under high volumes and pressures within the urinary bladder. With prompt bladder decompression, the hydronephrosis resolved and the patient had no untoward long-term effects from his transient renal obstruction.

Ureteral Obstruction

Similarly, the ureters are also subject to both benign and malignant obstructive processes – both intrinsic and extrinsic. The frequency at which these conditions affect one versus both ureters vary.

Non-malignant Extrinsic

Non-malignant extrinsic processes include traumatic obstruction, iatrogenic injury, crossing vessels, retroperitoneal fibrosis, and mass effect—most commonly due to the gravid uterus or similarly enlarged uterus from fibroids.

A 75-year-old woman presented after undergoing an anterior spinal fusion surgery with significant hardware implantation (Fig. 12.3). She developed massive right-sided hydronephrosis as evidenced by axial CT imaging. A nuclear scan revealed that the kidney was nonfunctional. The patient was having significant nausea and vomiting and still recovering from her anterior spinal fusion. She elected for ureteral stent placement. The collecting system was markedly dilated but after stent placement the hydronephrosis improved and her nausea symptoms dissipated. Key here is that even the nonfunctional kidney, when obstructed, can still cause significant symptoms. Relieving the obstructive process can improve the patient’s quality of life even without residual renal function to preserve.

In some cases, the diagnosis of obstruction is unclear. A 55-year-old woman presented with early satiety. She was found to have an extremely large left upper pole renal cyst compressing the stomach (Fig. 12.4). The patient was told by the referring provider that she had right-sided hydronephrosis as well, but on closer inspection, the hydronephrosis was actually a parapelvic cyst. These cysts can mimic hydronephrosis but are separate and unique from the collecting system which is often decompressed. Parapelvic cysts should be on the differential for hydronephrosis, especially in the asymptomatic patient with contralateral renal cystic disease. Retrograde pyelography or delayed images after intravenous contrast during CT imaging will help establish the diagnosis.

Occasionally ureteral obstruction can be idiopathic. For example, a 63-year-old woman presented with incidentally discovered left hydroureteronephrosis down to the level of the ureterovesical junction (Fig. 12.5). She had adequate bladder capacity on a cystography and retrograde pyelography revealed an extremely tortuous and convoluted ureter which had been chronically obstructed. In situations where the ureters are chronically obstructed, it can develop significant tortuosity and folding, making retrograde access complex. Establishing access is possible through the use of angled-tipped hydrophilic glide catheters as well as careful manipulation of the open-ended ureteral exchange catheter. The exchange catheter was advanced slowly over the wire until such time as further navigation became difficult and then the hydrophilic catheter is torqued and advanced. The angulated/kinked ureter can be straightened by pulling back gently on both the exchange catheter and wire simultaneously to create friction and counter-tension. Ultimately, after stent placement and ureteral biopsy (showing benign urothelial cells), the patient elected for laparoscopic ureteral lysis and psoas hitch reimplantation. Negotiating such complex ureters requires the availability and use of a variety of guidewires including hydrophilic, angle-tipped, floppy and stiff/super-stiff varieties.

Similar findings were noted in a patient with right-sided renal tuberculosis and left ureterovesical junction obstruction of unclear etiology (Fig. 12.6). The left ureter was extremely tortuous and dilated while the right ureter showed multiple filling defects consistent with renal tuberculosis. The patient underwent a right laparoscopic nephrectomy for renal tuberculosis and is currently being managed with stent changes for her left hydroureteronephrosis. Chronic stent changes require plastic (to be changed every 3–4 months) versus metal varieties that can be left indwelling for up to 1 year. Such stent changes frequently can be performed under local anesthesia with fluoroscopic guidance.

Ureteropelvic junction obstruction is a common etiology for unilateral (or even bilateral [Fig. 12.7]) renal obstruction. Workup includes functional nuclear imaging and, in some cases, cross sectional arteriography to evaluate for a blood vessel crossing over the anterior aspect of the ureteropelvic junction. A complete description of evaluation and management of ureteropelvic junction obstruction is beyond the scope of this chapter.

Non-malignant Intrinsic

Non-malignant intrinsic causes can include obstructing ureteral stones, ureteral strictures, congenital ureteropelvic junction obstruction, infection and fibroepithelial polyps among others.

A representative case involves a 68-year-old female with a long mid-ureteral stricture which developed after a series of complicated ureteroscopy procedures performed for obstructing calculi (Fig. 12.8). The patient ultimately developed a complete obstruction; retrograde imaging combined with antegrade nephrostography illustrated that the ureter was obliterated from the entire middle third. The patient’s GFR was approximately 28 mL/min and she had 34% split renal function on nuclear imaging on the affected side. This patient elected for management with a laparoscopic donor nephrectomy followed by an auto-transplantation of the left kidney to the left pelvis to avoid potential dialysis. In cases where marginal renal function would preclude an ileal ureteral substitution due to electrolyte abnormalities, long or proximal ureteral defects, and/or preservation of existing renal function is critical to avoid dialysis, laparoscopic donor nephrectomy with auto-transplantation offers an excellent management option.

Next consider the case of a 56-year-old female who presented with an infected ventriculoperitoneal shunt (Fig. 12.9). She was incidentally discovered to have bilateral “obstructing” ureteropelvic junction calculi and severe hydronephrosis on CT imaging. The patient was producing urine, had normal renal function, and had no flank pain. Given the dilation of the collecting system and the impacted appearance of the stones on CT imaging, the patient elected for bilateral simultaneous percutaneous nephrolithotomies. She was rendered stone free after one procedure. Figure 12.9 reveals that the kidneys had excellent initial uptake of contrast on CT images and her normal renal function suggested that even though the kidneys were “obstructed”, remarkably they are still functioning normally. The patient was not having any pain from her “obstructing” stones. Acute urinary obstruction without radiographic evidence of obstruction can result in severe pain while chronic obstruction with slow dilation may be associated with an asymptomatic patient. History along with appropriate imaging will help direct therapy.

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