bubble_chart Overview

Obstructive nephropathy refers to a disease caused by urinary flow obstruction leading to renal function and parenchymal damage. This condition can occur acutely or chronically, and the lesions are often unilateral, but in many cases, they can also be bilateral. Urinary tract obstruction is usually a significant cause of obstructive nephropathy, but if the obstruction does not affect the kidney parenchyma, it is generally not referred to as obstructive nephropathy but rather as obstructive uropathy. Hydronephrosis is often a clinical finding in obstructive nephropathy, but many cases of obstructive nephropathy (such as intrarenal obstruction) do not necessarily present with hydronephrosis. Additionally, many conditions, particularly congenital ureteral abnormalities, may show renal pelvis dilation upon examination but not necessarily hydronephrosis.

bubble_chart Etiology

The main causes of urinary tract obstruction can be divided into two categories: those related to the ureter itself and those external to the ureter. Ureteral causes are further divided into intraluminal obstruction and ureteral wall disorders. Stones are the most common cause of intraluminal obstruction and can occur anywhere in the ureter, but are most frequent at the three natural turns or narrowings. They can also occur within the small tubules of the kidney. Renal stones are often caused by various metabolic disorders, commonly due to uric acid crystals or the use of poorly soluble sulfonamide drugs. In some cases of multiple myeloma, large amounts of Bence-Jones protein can deposit in the renal tubules, causing obstruction. In cases of renal papillary necrosis, necrotic tissue can slough off and cause obstruction. Additionally, blood clots formed from urinary system bleeding can also obstruct the urinary tract, with the latter two situations mostly occurring outside the kidney.

Ureteral wall disorders can be functional or anatomical abnormalities. Functional disorders often result from abnormal peristalsis of the ureteral muscles, either the longitudinal or circular muscles, preventing normal urine flow. These are more common at the ureteropelvic junction and are often bilateral in children, with the left kidney usually more severely affected, making the symptoms more pronounced. Another group involves disorders at the ureterovesical junction, more common in males and usually unilateral. In both cases, there is often a lack of longitudinal muscle fibers while the circular muscles remain relatively normal. Previously, it was thought that the mechanism was similar to that of megacolon, but now most believe the mechanisms are different.

Bladder dysfunction leading to urinary obstruction is mostly neurogenic, caused by congenital muscle hypoplasia or spinal cord dysfunction. Acquired causes are commonly seen in diabetes, cerebrovascular disease, multiple sclerosis, or Parkinson's disease.

Anatomical changes due to sexually transmitted diseases can cause ureteral wall lesions, including inflammation and tumors, leading to narrowing.

Obstruction external to the urinary tract is often caused by disorders of the reproductive system, gastrointestinal system, or vascular or retroperitoneal diseases. Enlarged prostate or tumors are common causes in males. In females, it is often due to uterine or ovarian disorders. Crohn's disease or other gastrointestinal tumors can compress the ureter, causing obstruction. Retroperitoneal diseases can be caused by inflammation or tumors (primary or metastatic).

bubble_chart Pathogenesis

The manifestations vary depending on the speed of obstruction onset, whether it is unilateral or bilateral, and the degree of obstruction completeness. However, regardless of the above circumstances, the following pathophysiological changes always occur.

(1) Increase in ureteral pressure: This generally occurs very quickly, and if the urine volume is large, the pressure rises even faster. Excessive intraluminal pressure can promote lumen dilation and strengthen peristalsis. If the obstruction is mild, the increased intraluminal pressure can sometimes overcome the obstruction partially on its own due to the dynamic action of peristalsis. The normal intraluminal pressure of the ureter is about 0.8～1.33kPa (6～10mmHg). In cases of significant obstruction, this pressure can sometimes reach 5.33～6.67kPa (40～50mmHg). In many cases of obstruction caused by congenital disorders, although the intraluminal pressure of the ureter is usually high, it can often be maintained within a certain stable range. Once acute new-onset obstruction occurs, it can cause a significant increase in intraluminal pressure, leading to significant renal dysfunction.

(2) Changes in renal hemodynamics: In animal experiments, acute bilateral obstruction can initially cause a brief increase in renal blood flow, but it decreases thereafter (about 1 hour later), and the glomerular filtration rate (GFR) decreases. This is due to the increase in intratubular pressure directly opposing the filtration pressure in the glomerulus. In chronic bilateral obstruction, the renal plasma flow can generally be maintained at a certain level, about 60～70% of normal. Although the tubular fluid cannot be excreted through the ureter and other pathways, the renal tubules can still reabsorb much of the filtered fluid, so the GFR does not completely drop to zero. The impact of unilateral obstruction on renal hemodynamics also depends on the speed of onset. In acute cases, GFR decreases, proximal tubular pressure can be normal, and changes in renal plasma flow (RPF) may not be very significant. Additionally, the contralateral RPF may increase compensatorily, possibly due to the activation of the renorenal reflex. In chronic unilateral ureteral obstruction, the intraluminal pressure is generally not as high as in acute cases, and the proximal tubular pressure usually decreases, about 30% of normal. Due to chronic obstruction, various compensatory mechanisms are often exhausted, so RPF generally decreases, about 40% of normal.

(3) Tubular function: If the obstruction is only partial and not complete, the main dysfunction occurs in the distal tubules. This is manifested as a disorder in the kidney's ability to concentrate urine. In a few cases, the dysfunction in concentrating ability can be very significant, mainly due to increased blood flow in the non-obstructed medullary region after partial obstruction, which removes the high osmotic gradient and solutes from the renal medullary interstitium. Additionally, excessively high intratubular pressure can affect the thick ascending limb of Henle's loop, particularly the NaCl transport in the juxtamedullary nephrons, affecting the countercurrent multiplication effect. Furthermore, due to the pressure on the collecting ducts, the cells there may respond abnormally to vasopressin, which is also a mechanism. Some cases may also manifest as impaired sodium reabsorption, leading to salt loss. Tubular acidification function can also be impaired in long-term obstruction cases, manifesting as high urine pH and metabolic acidosis.

After the obstruction is relieved, the following changes in renal function may occur:

1. GFR and RBF: RPF generally gradually increases after the obstruction is relieved, but because the blood is mostly redistributed to the medulla, the actual increase is not significant, and in some cases, it may even be less than before. Some believe that the renal tissue often secretes more thromboxane A₂, which significantly reduces cortical blood flow. GFR generally remains unchanged for a considerable period, and in some cases, it may slightly increase later. Animal experiments have shown that after a long period of complete obstruction, even after the obstruction is relieved, GFR usually takes about 2～6 months to recover to its limit. Most cases do not fully recover, with most only recovering to about 50% of the original level.

2. Renal Tubular Function Abnormalities in concentrating function can generally persist for a long time. Animal micropuncture experiments have found that at this time, water reabsorption in the proximal tubule, Henle's loop, and distal tubule is reduced. Many experiments have confirmed that there are cAMP production disorders in the distal tubule; impaired response to PTH; H⁺ secretion and HCO₃¹ reabsorption disorders; Na⁺-K⁺-ATPase, Mg²⁺-ATPase disorders; ATP production disorders; and many metabolic disorders such as glucose oxidation, gluconeogenesis, etc.

bubble_chart Pathological Changes

In the early stages, the primary manifestation is the dilation of the renal tubule lumens, predominantly in the collecting tubules and other distal tubules, mainly due to increased intraluminal pressure. Over time, the epithelial cells of the renal tubules become flattened and gradually atrophy, with the pathology extending from the distal to the proximal tubules. In the early stages, glomerular lesions are not prominent, but Bowman's capsule may dilate, and inflammatory cell infiltration and fibrosis gradually appear around the glomeruli. As the disease progresses, renal pathology becomes more complex, with more pronounced chronic inflammatory cell infiltration in the tubulointerstitium, possible complete collapse of the glomeruli, sclerotic changes, and similar alterations in the renal vasculature. In the advanced stage, due to factors such as hypertension, renal pathology can sometimes be difficult to distinguish from that induced by other chronic glomerulonephritis. However, since the lesions in this disease are often asymmetrical, this can serve as a diagnostic criterion for the disease cause.

bubble_chart Clinical Manifestations

Based on the fundamental disease causes, the symptoms can vary depending on the degree of obstruction and the duration of the disease. The following groups of symptoms often appear:

(1) Pain - The typical manifestation is renal colicky pain, which can be persistent but often exacerbates paroxysmally and radiates to the perineum. However, in patients with chronic obstructive nephropathy that develops gradually, pain may not always be prominent, and occasionally only manifests as lumbar discomfort. The kidney volume can significantly enlarge in acute obstructive nephropathy, but in chronic cases, due to the proliferation of fibrous tissue, the volume may not necessarily increase, and in many cases, the affected kidney may even atrophy.

(2) Urinary disorders - Bilateral complete obstruction can lead to anuria, but in most patients with this disease, the obstruction is not entirely complete, thus often presenting as polyuria, the mechanism of which has been previously mentioned. In cases of recurrent episodes, anuria may occur during the episodes, with polyuria manifesting during the intervals. In cases of obstruction caused by infection, bladder irritation symptoms may appear, and in cases caused by bladder neck obstruction (such as prostatic hypertrophy), urinary retention may be present.

(3) Hypertension - Quite common, the mechanism may be due to excessive renin secretion caused by excessively high pressure in the renal tubules or interstitial pressure; it may also be due to the kidney's impaired regulation of water and sodium, leading to water and sodium retention and resulting in hypertension. Generally, hypertension caused by unilateral renal disease leading to this condition is mostly renin-dependent, while that caused by bilateral disease is mostly water-sodium dependent. Hypertension generally improves after the obstruction is relieved. However, if the disease has been present for a long time, hypertension may sometimes persist for a considerable period.

(4) Polycythemia - Mainly due to excessive secretion of erythropoietin stimulated by hydronephrosis. After surgical correction of the obstruction, the excessively high hematocrit can decrease. However, clinically, not many cases truly present with typical symptoms of this condition.

(5) Acidosis - Mainly due to the effect on the secretion of H⁺ by the renal tubules. Some cases may be accompanied by hyperkalemia.

bubble_chart Diagnosis

Urinalysis, ultrasound, and X-ray examinations can not only establish a diagnosis but also clarify the disease cause.

The urine volume in urinalysis has been mentioned earlier. The routine may vary depending on the disease cause. Most cases present with proteinuria, but the amount is generally not significant. Red and white blood cells are often observable. In cases caused by stones or tumors, the number of red blood cells can be substantial, sometimes leading to gross hematuria; if infection is present, there may be an increased number of white blood cells. In cases caused by renal papillary necrosis, the urine may contain not only a higher number of red blood cells but also a significant number of white blood cells. The typical urine color in such cases resembles "meat-washing water," and necrotic tissue can be seen after filtering through red gauze. Cast examination often suggests the disease cause, such as crystals from sulfonamides or uric acid adhering to the casts. In cases with concurrent infection, the urine pH is often elevated; a persistent pH above 7.5 mostly indicates long-standing obstruction and a more chronic condition.

Besides measuring kidney size, B-ultrasound can also detect hydronephrosis and many stones. If a significant amount of residual urine is found in the bladder after voiding, it suggests prostatic hypertrophy, tumor, or neurogenic causes.

Abdominal plain films can detect positive urinary stones; calcifications in the abdominal cavity and renal area can be seen in cases caused by subcutaneous node bacilli, and kidney size can also be roughly observed. CT can measure kidney size and detect whether there is dilation of the collecting duct system. It is particularly important for diagnosing cases caused by tumors (intrarenal or extrarenal) or retroperitoneal lesions. A small number of special cases require retrograde ureterography for imaging. In some cases of acute obstruction, intravenous pyelography can help clarify the disease cause.

bubble_chart Treatment Measures

The removal of stones can be achieved through shock wave lithotripsy, depending on the disease cause, and is generally more effective for stones sized between 7 to 15 mm. For stones in the middle and lower segments of the ureter that do not respond to conservative treatments (such as increased water intake and Chinese medicinals), a retrograde stone extraction method under bladder mirror should be employed. In cases where kidney function is affected or the aforementioned methods are unsuccessful, surgical removal is necessary. Antibiotics are often required concurrently. Many cases of obstructive nephropathy are not completely obstructed, but secondary infections can lead to edema, inflammatory secretions, and more pronounced obstruction. After antibiotic treatment, the obstruction can significantly improve, but the dosage and choice of medication should be adjusted based on culture results and kidney function. For cases caused by tumors, chemotherapy or surgical intervention is required. Post-obstructive polyuria and resulting water and electrolyte imbalances should be promptly corrected.