Polycystic kidney is characterized by numerous cysts of varying sizes within the kidney parenchyma, some large enough to be very sizable and others barely visible to the naked eye. These cysts cause the entire kidney to enlarge, with a surface marked by uneven cystic protrusions. The cysts contain a pale yellow serous fluid, which may appear dark brown or reddish-brown due to hemorrhage. The fluid contains urea, uric acid, creatinine, proteins, phosphates, and shed epithelial cells. Polycystic kidney is not a rare condition, with literature reporting approximately one case in every 250–300 autopsies. It typically affects both kidneys, with unilateral occurrence being extremely rare. The incidence is equal between males and females, and it can occur at any age, though most cases are diagnosed between 40 and 60 years. The disease has a familial hereditary tendency, but accompanying congenital malformations in other organs are uncommon.

bubble_chart Etiology

The true cause of polycystic kidney disease is not entirely clear, and several theories have been proposed: 1. **Metabolic Theory**: This suggests that during the embryonic stage, salt deposits block the renal tubules, causing fluid accumulation in the proximal segments and leading to cyst formation. 2. **Infection Theory**: Scholars represented by Virchow believe that embryonic pyelonephritis causes fibrosis of the renal tubules, resulting in obstruction and subsequent cyst formation. 3. **Neoplastic Theory**: Since polycystic kidneys often present as actively growing masses, some consider it a true neoplasm. Staemnier once referred to it as "cystadenoma fibromatosis." 4. **Developmental Defect Theory**: This posits that during embryonic development, the connection between the renal tubules and collecting ducts (or between the straight tubules and renal calyces) is interrupted either partially or completely, halting kidney development. This obstruction in urine excretion leads to retention cysts in the glomeruli and renal tubules. Currently, most scholars support the last theory.

The size of polycystic kidneys is significantly larger than that of normal kidneys, sometimes up to five or six times larger. The surface is covered with cysts of varying sizes, making it extremely uneven. The cyst walls do not connect with each other or with the renal pelvis. The inner surface of the cyst walls is lined with cuboidal epithelium, and many glomeruli show hyaline degeneration. Renal function gradually declines, and the walls of the renal tubules become sclerotic. Consequently, the majority (approximately 60–75%) of patients develop hypertension. The aforementioned features—cyst size, decline in renal function, and the onset of hypertension—are all progressive. Therefore, patients often exhibit no symptoms in their early years, but the incidence of the disease gradually increases after the age of 40.

bubble_chart Clinical Manifestations

The clinical manifestations of polycystic kidney disease can be divided into three types: The first type involves the discovery of a mass in the upper abdomen or localized distending pain and gastrointestinal symptoms due to compression by the mass. The second type includes symptoms of renal insufficiency such as facial edema, dizziness, and nausea. The third type presents with dizziness, headaches, hypertension, accompanied by physical weakness, anemia, and weight loss. Generally, patients do not experience difficulty in urination or changes in urine, but minor lumbar trauma may lead to hematuria.

bubble_chart Diagnosis

In addition to the aforementioned clinical manifestations, the diagnosis of this disease primarily relies on pyelography. The pyelogram reveals characteristic deformities, malformations, defects, and elongation of the calyceal necks caused by compression from multiple cysts. Specifically, multiple indentations are observed on the renal pelvis and calyces, and these changes are often bilateral. Furthermore, ultrasound examination shows enlargement of both kidneys with multiple fluid-filled segments. The iodine¹³¹

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bubble_chart Treatment Measures

In the past, no active treatment measures were taken for this disease, and only supportive treatments such as a low-salt, low-protein diet, avoiding excessive strenuous activities, and preventing any infections or injuries were employed. Although these measures were beneficial for protecting kidney function, they ultimately lacked proactive significance. In recent years, for early diagnosed cases, decompression surgery has often been actively adopted, yielding certain results. When complications such as obstruction, stones, infections, or severe compression symptoms arise, surgical intervention must be considered, including procedures to relieve obstruction, remove stones, drain infections, or perform decompression surgery by excising overly large cysts. The prognosis for this disease is poor. In the past, adult patients diagnosed with this condition typically had an average survival period of around 10 years, and once uremia developed, survival rarely exceeded 5 years. Nowadays, for early-stage cases, active decompression surgery is employed, while advanced-stage cases are treated with dialysis or kidney transplantation, significantly improving the prognosis compared to the past.

bubble_chart Prognosis

The prognosis of this disease is poor. In the past, the average survival time after diagnosis in adult cases was generally around 10 years, and once uremia develops, the survival period often does not exceed 5 years.