Search

BACKGROUND Hemodialysis corrects metabolic acidosis by transferring bicarbonate or bicarbonate equivalents across the dialysis membrane from the dialysis fluid to the plasma. With the conventional three-stream bicarbonate-based dialysis fluid delivery system, a change in the bicarbonate concentration results in changes in the other electrolytes. In practice, the dialysis machine draws either a little less or more from the bicarbonate concentrate and a little more or less from the acid concentrate, respectively in a three-stream delivery system. The result not only changes the bicarbonate concentration of the final dialysis fluid but also causes a minor change in the other ingredients. METHODS We propose a four-stream bicarbonate-based dialysis fluid delivery system consisting of an acid concentrate, a base concentrate, a product water, and a new sodium chloride concentrate. RESULTS By adjusting the flow rate ratio between the sodium chloride and sodium bicarbonate concentrates, one can achieve the desired bicarbonate concentration in the dialysis fluid without changing the concentration of sodium or ingredients in the acid concentrate. The chloride concentration mirrors the change in bicarbonate but in the opposite direction. CONCLUSION A four-stream, bicarbonate-based dialysis fluid delivery system allows the bicarbonate concentration to be changed without changing the other constituents of the final dialysis fluid.

PURPOSE OF REVIEW: The novel corona virus (SARS-CoV2) has been demonstrated to cause acute kidney injury due to direct cellular toxicity as well as due to a variety of autoimmune glomerular diseases. The concept of a surge of infected patients resulting in an overwhelming number of critical patients has been a central concern in healthcare planning during the COVID-19 era. RECENT FINDINGS: One crucial question remains as to how to manage patients with end stage renal disease and acute kidney injury in case of a massive surge of critically ill infected patients. Some publications address practical and ingenious solutions for just such a surge of need for renal replacement therapy. We present a plan for using a blood pump, readily available dialysis filter, and a prefilter and postfilter replacement fluid set up. This is in conjunction with multiple intravenous pumps to develop a simple hemofiltration apparatus. SUMMARY: The current set up may be a readily available option for use in critical situations where the need for renal replacement therapy outstrips the capacity of traditional hemodialysis services in a hospital or region.

Patients with advanced chronic kidney disease have an inability to excrete phosphorus normally leading to high serum concentrations of phosphorus. The hyperphosphatemia is even more pronounced in dialysis patients who often require large doses of phosphorus binders to combat the problem. Hemodialysis is able to remove fair amount of the extra phosphorus; however, the removal is often hampered by the fact that the phosphorus is removed only from the extracellular compartment and phosphorus is mainly intracellular. The end result being a high serum phosphorus concentration at the beginning of dialysis, a sharp decline in the value by the end of dialysis and significant rebound of serum phosphorus concentration a few hours after stopping dialysis as phosphorus moves out of the cells. Here, we describe 2 hemodialysis patients with normal predialysis serum phosphorus concentration and preexisting conditions that made them at risk for developing encephalopathy who developed recurrent obtundation toward the end of the dialysis treatments. After confirming critical postdialysis hypophosphatemia, phosphorus was added to the dialysate baths and the episodes of encephalopathy associated with dialysis ceased.

Background AA amyloidosis due to subcutaneous injection of drugs of abuse has been described in the USA, but all the existing literature is from more than 20 years ago. There is more recent literature from Europe. We have observed a high incidence of AA amyloidosis in the county hospital in San Francisco. Design Here, we describe 24 patients who had kidney biopsy-proven AA amyloidosis from our hospital from 1998 to 2013. All the patients were thought to have AA amyloidosis from skin popping of illicit drugs after having exhausted the intravenous route. These patients with biopsy-proven AA amyloidosis were analysed further. Results All patients were found to have hepatitis C infection, hypertension was not common, most had advanced kidney failure, and acidosis was common as was tubulointerstitial involvement on the kidney biopsy. Other organ involvement included hepatomegaly and splenomegaly in a number of patients; direct myocardial involvement was not seen, but pulmonary hypertension, history of deep vein thrombosis and pulmonary embolism were common. The prognosis of these patients was poor. The mortality rate approached 50% 1 year after biopsy, and most of the patient needed dialysis shortly after diagnosis. Cessation of drug use seemed beneficial but rarely achievable. Conclusion AA amyloidosis from skin popping is common in San Francisco. Most patients with renal involvement end up on dialysis, and mortality rates are exceedingly high.

It is generally believed that significant renal ablation leads to hyperfiltration and eventually progressively worsening chronic kidney disease. The data behind this belief have not been scrutinized intensively. More importantly, the above belief leads many physicians to manage patients differently than they otherwise would manage. Here, we examine the data behind whether hyperfiltration occurs when patients lose kidney mass (by excision or by disease) and whether the hyperfiltration is uniformly injurious.

Membranous glomerulonephritis is most often idiopathic, but it can be secondary to systemic lupus erythematosus, viral hepatitis, and drugs. A number of malignancies have also been associated with membranous glomerulonephritis, although a causal link has not been established yet. A young patient with lymphangioleiomyomatosis is described who developed massive proteinuria and was found to have membranous glomerulonephritis on renal biopsy. There were many pathological features and some clinical features that suggested the patient also suffered from systemic lupus erythematosus.

The bone morphogenic protein (BMP) antagonist gremlin was highly expressed in the cellular and fibrocellular crescents of 30 renal biopsies of patients with pauciimmune glomerulonephritis—as well as in renal tubular and infiltrating interstitial cells. It correlated with tubulointerstitial fibrosis and co-localized with transforming growth factor beta (TGF-β), suggesting that it may be important in mediating some of its pathological effects (Nephrol Dial Transpl 22: 1882). Soluble F11 receptor (F11R) is elevated in dialysis patients and may be yet another marker of increased cardiovascular risk. It is a cell adhesion molecule expressed on the membrane surface of platelets and related to the murine protein present in the tight junctions of the vascular endothelium. In activated platelets F11R becomes phosphorylated and causes cell adhesion and aggregation—the initial step of thrombus formation in the pathogenesis of atherosclerotic plaques (J Invest Med 55:115). In order to study the mechanism of renal injury from light chains, cell cultures of human proximal cells were incubated with light chains derived from the urine of patients with multiple myeloma. This resulted in the cells producing hydrogen peroxide and monocyte chemo-attractant protein-1, both inherently nephrotoxic (J Am Soc Nephrol 18:1239). The use of estimated glomerular filtration rate (GFR) derived from the serum creatinine concentration is fraught with pitfalls. It tends to undererestimate renal function in persons with no known kidney disease and overestimate it in emaciated patients with low muscle mass and reduced creatinine production. Also problematic is its use in acute renal failure, where the change in serum creatinine is more important (BMJ 334:1198, Nephrol Dial Transplant 22:2391). Subjects in the Framingham study who had both microalbuminuria and reduced eGFR had worse cardiovascular outcomes than those with only one of these abnormalities (Arch Int Med 167:1386 2007). A study of type II diabetics with nephropathy found that simvastatin, unlike cholestyramine, appears to stabilize GFR, possibly by increasing messenger RNA expression of slit diaphragm associated proteins and reducing the albumin excretion rate (Kidney Int 70:177–186). The administration of iodine containing contrast media to a hemodialysis patient resulted in so-called iodine gout, an acute and dramatic swelling of the thyroid and salivary glands. This rare idiosyncratic complication may be related to toxic accumulation of iodide in the salivary gland ducts. The patient improved dramatically within 48 h of high-dose prednisolone therapy (Nephrol Dial Transpl 22: 1250)

A high incidence of hypervolemic hypernatremia has been described in patients recovering from acute kidney injury (AKI) in intensive care units. However, this has been limited to only a few cases. One hundred fifty adult patients recovering from AKI in the intensive care unit of a single institution during a 6-year period, who developed hypernatremia during the course of their illness, were investigated. Serum and urine electrolytes, osmolality, urea nitrogen and creatinine were measured. The weights of these patients at the time of hypernatremia development and at presentation to the hospital were also measured. Even though the hypernatremia was mild in most patients (146–160 mEq/L), the average rise in serum sodium concentration was 14.5 ± 7.1 mEq/L. Of the 34 patients who had all urinary studies available, the average urine osmolality was 436 ± 128 mmol/kg of which 172 ± 54 mmol/L was contributed by sodium, potassium and their accompanying anion. Another 204 ± 96 mmol/L was accounted for by urea and creatinine (mainly urea). Almost all the patients had hypervolemia as evidenced by the presence of edema and an average weight gain of more than 9 ± 11 kg between the time of presentation and the onset of hypernatremia despite likely having lost muscle mass from being in the intensive care unit for several days. The weight data were available in 54 patients, and only eight of these patients had lost weight at the time of the development of hypernatremia. Hypervolemic hypernatremia is by far the most common cause of hypernatremia in patients in the intensive care unit. Even though the patients are in negative fluid balance at the time of the development of the hypernatremia, earlier saline administration has caused massive volume overload despite the ongoing losses. Post-AKI diuresis in the face of inability to maximally concentrate the urine because of renal failure often leads to mainly mild elevations in serum sodium concentration. The urine solute is mainly urea because of the often high serum urea concentrations with little electrolytes being present in the urine.

Background: The clinical significance of a trace protein reading on urinalysis is unclear, and such a result is often ignored by the clinician. Methods: We examined 185 samples of urine with trace proteinuria by both Chemstrips and sulfosalicylic acid testing, and compared the results with those of urinary albumin and total protein concentrations. Results: Taking for the purposes of this study an arbitrary upper limit of normal of 20 mg/l for albumin and 100 mg/l for total protein concentration, we found abnormal albumin excretion in 87% and abnormal total protein excretion in 88% of trace samples. In this study, a negative urinalysis for protein excluded microalbuminuria in 87% and proteinuria in 78% of cases. Conclusion: Qualitative testing for protein by urinalysis has a high sensitivity and specificity for diagnosing or ruling out microalbuminuria. Trace proteinuria usually means microalbuminuria; negative proteinuria tends to rule it out.

An aggressive dialysis in a grossly azotemic patient, especially one with severe metabolic acidosis, can lead to dialysis disequilibrium syndrome (DDS). Mild forms present as nausea, vomiting, restlessness, and headache. Severe manifestations include seizures, obtundation, coma, and even death. This clinical picture is caused by cerebral edema induced by one or more of the following mechanisms: "Reverse urea effect" - Dialysis removes urea faster from the blood than from the brain; consequently, water enters the brain. "Cerebrospinal fluid acidosis" - Correction of systemic acidosis engenders the condition due to a lowering of brain pH. "Idiogenic osmoles" - As a response to blood hyperosmolar state, osmoles are produced in the brain. As blood osmolality decreases under relatively quick dialysis, idiogenic osmoles tend to induce brain edema. Because the symptoms of DDS can be life-threatening, preventive measures in patients with severe uremia are important. The first strategy relies on raising blood osmolality by introducing solutes (osmoles) into the blood. The second approach, which is the most common, decreases the efficiency of the dialysis treatment by shortening the duration of a dialysis run to 25% - 30% of normal, by lowering dialyzer blood flow or dialysate flow rate, by using a less efficient dialyzer, or by a combination of these maneuvers. Dialysis frequency is increased instead. Anticonvulsant drugs are needed in cases where the preventive measures have not been used or have been unsuccessful.

Membranous glomerulonephritis is typically classified as idiopathic or secondary to systemic lupus erythematosus (SLE), hepatitis B, drugs, toxins, other infections, or malignancy. Not infrequently in some patients without a definite diagnosis of SLE, pathologic features of secondary membranous nephropathy are seen e.g., mesangial and/or subendothelial deposits, tubuloreticular inclusions, and full house immunofluorescence. In these patients, there is uncertainty about the etiology, response to therapy, and prognosis of membranous GN. We retrospectively reviewed the charts of 98 patients with membranous GN at San Francisco General Hospital and John Stroger Hospital of Cook County over a 10-year period. Data were collected and analyzed using SPSS.18. Thirty-nine (40 %) had idiopathic membranous GN (Group 1), thirty-six (37 %) had lupus membranous GN (Group 2) and twenty-three (23 %) had some pathological features of secondary membranous GN, but no definite etiology of membranous GN (Group 3). At baseline (at time of renal biopsy) and after mean follow-up of 3.5 years, the average serum creatinine (in mg/dL) in Group 1 was (1.6 ± 1.0 versus 1.6 ± 1.7), Group 2 was (1.8 ± 2.5 versus 1.2 ± 0.9) and Group 3 was (1.1 ± 0.4 versus 1.27 ± 0.83), respectively. For the same time points, the average urine protein to creatinine ratio (g/g) in Group 1 was (9.8 ± 7.1 versus 5.7 ± 6.7), Group 2 was (4.2 ± 3.9 versus 1.7 ± 2.2), and Group 3 was (7.4 ± 5.7 versus 3.1 ± 3.8). In addition, during the follow-up period, eleven of 39 (28 %) in Group 1, two of 36 (6 %) in Group 2, and three of 23 (13 %) in Group 3 progressed to end-stage renal disease and were started on dialysis. It appears that patients with lupus membranous GN have better renal prognosis than patients with idiopathic membranous GN. The renal prognosis for patients with pathological features of lupus membranous but no diagnosis of systemic lupus (lupus-like membranous GN) falls in between. Further studies are needed to determine if Group 3 patients can (a) definitively be classified as true idiopathic membranous GN or lupus membranous GN or (b) they have a separate disease from either M-type phospholipase A2 receptor membranous nephropathy or systemic lupus-induced membranous nephropathy.

Insulin-like growth factor-binding protein-1 (IGFBP-1) is produced by the liver and regulated by glucocorticoids and insulin at the level of gene transcription. To identify DNA sequences mediating the effects of glucocorticoids and insulin on IGFBP-1 promoter activity we created luciferase reporter gene constructs and performed transfection studies in H4IIE hepatoma cells. Initial studies confirmed that the IGFBP-1 promoter is functional when inserted in the correct orientation, but not in the reverse orientation. Dexamethasone (DEX) increased promoter activity 10-fold, and insulin reversed this effect of DEX by 85% at 8 h. The effects of DEX were abolished when constructs were truncated to 89 bases from the RNA cap site, and DNase footprinting with the DNA-binding domain of the human glucocorticoid receptor identified an imperfect palindrome containing two receptor-binding sites separated by three nucleotides typical of a glucocorticoid response element (GRE) at this location. Mutation of either binding site (or half-site) disrupted the effects of DEX, confirming that this sequence functions as a GRE. Two other regions of the promoter also footprinted with the glucocorticoid receptor protein and contained sequences consistent with glucocorticoid receptor-binding sites; however, neither of these footprints contained the full structure expected of a functional GRE, and neither mutation nor deletion of these other sequences altered the effects of DEX on promoter activity. To identify the DNA sequences required for the effects of insulin on glucocorticoid-stimulated promoter activity, we created internal deletions throughout the IGFBP-1 promoter region. Deletion of the 22-basepair (bp) sequence immediately 5' from the GRE disrupted the effect of insulin and appeared to increase basal promoter activity at least 2-fold in each of eight experiments (P < 0.001 vs. intact promoter). This region of the IGFBP-1 promoter contains a 19-bp palindrome (CAAAACAAACTTATTTTG) that overlaps the 5'-end of the GRE and is fully conserved in the human IGFBP-1 promoter. Each half of this palindrome resembles previously identified insulin response sequences, and deletion/mutation analysis suggests that each half may contribute to the effects of insulin on promoter activity. Gel shift studies confirmed that this palindrome binds H4IIE nuclear proteins. In summary, we have identified a GRE in the 5'-promoter region of the rat IGFBP-1 gene approximately 90 bp up-stream from the RNA cap site as well as a contiguous 22-bp region that plays a critical role in mediating the effects of insulin on glucocorticoid-stimulated promoter activity.(ABSTRACT TRUNCATED AT 400 WORDS)

Expeditious diagnosis of peritonitis remains a significant goal in the management of patients maintained on peritoneal dialysis. Several attempts to use leukocyte esterase reagent strips to diagnose peritonitis have been described. In this study we examined the usefulness of a new reagent strip, the PeriScreen Test Strip, in the diagnosis of peritonitis. A series of 72 peritoneal effluent samples obtained from 22 maintenance peritoneal dialysis patients is reported. In this study, the test strips had a sensitivity of 100% and a specificity of 98.3% as compared to an abnormal leukocyte count. Thus, in the diagnosis of peritonitis we believe that the PeriScreen Test Strip can be used as a simple bedside screening test to exclude peritonitis in peritoneal dialysis patients.

A high incidence of hypernatremia is often observed in patients recovering from acute kidney injury (AKI) in intensive care units.An unselected cohort of 20 adult patients recovering from AKI in the intensive care unit of a single institution during a 1-year period, were investigated. Serum and urine electrolytes, osmolality, urea nitrogen and creatinine were measured in an attempt to determine the cause of the hypernatremia.Eighty-eight percent of patients who could not drink fluids were found to have hypernatremia (serum Na145 mEq/L). Even though the hypernatremia was mild in most patients (146-160 mEq/L), the average rise in serum sodium concentration was 17.4 mEq/L. The average urine osmolality was 384 mmol/kg of which 47.6 and 32.8 mmol/kg were contributed by sodium and potassium, respectively. The patients had hypervolemia as evidenced by the presence of edema and an average weight gain of 21.5 kg at the onset of the hypernatremia. The rise in serum sodium level coincided with an increase in urine output.The hypernatremia is believed to be due to post-AKI diuresis in the face of inability to maximally concentrate the urine because of renal failure. The diuresis caused a disproportionate loss of water in excess of that of sodium in the absence of replenishment of the water loss. Additionally, the patients were hypervolemic due to the retention of large quantities of sodium and water as a result of infusion of substantial volumes of physiological saline prior to the development of hypernatremia.

Foscarnet is an antiviral agent widely used in the treatment of cytomegalovirus (CMV) infection. We describe a cardiac transplant patient, who while being maintained with hemodialysis because of tobramycin-induced acute renal failure, was given Foscarnet for disseminated CMV infection. Using dialysate-side clearance methodology, we found the dialyzer clearance of Foscarnet to be in the order of 89 ml/min. (Int J Artif Organs 2000; 23: 165–7)

Low-grade chronic hemolysis is common in uremia, as red blood cell life span is clearly decreased with reduced renal function. Using isotope red cell tagging, it has been shown that red cell life span averages about 1/2 to 1/3 of normal in uremia. In addition, uremic erythrocytes have been found to be less deformable and osmotically more fragile when compared to their normal counterparts. Transfusion of uremic erythrocytes into an individual with normal renal function will restore the life span of those cells to normal. On the other hand, normal erythrocytes transfused into a uremic individual will have shortened survival. In the past, chronic hemolysis in maintenance dialysis patients may have manifested as increased blood transfusion require-ments. However, these days such hemolysis probably more often presents itself as erythropoietin resistance (larger erythropoietin doses being required for a given therapeutic response). A variety of abnormalities (such as impairment of red cell enzymatic activities and reduced synthesis of Na+ - K+ pump units by uremic reticulocytes) have been suggested to be the causes for the heightened predisposition of uremic erythrocytes to hemolysis. Uncommonly, patients on dialysis can have severe (at times life-threatening) hemolysis. These patients fit into either of two categories, depending on whether hemolysis involves all or the majority of the patients being dialyzed under similar circum-stances in a given dialysis center or whether the hemolysis is patient specific. Hemolysis in the former is often the result of water-borne toxins, centralized dialysis equipment failure, or blood tubing defects—whereas in the latter it results from medication or possibly inadequate dialytic therapy. Use of constricted blood tubing systems and of hypo-osmolal or abnormally warm dialysate results in intravascular hemolysis, whereas drug-induced hemolysis is usually extravascular.

Although patients with burns are known to develop hypocalcemia, the development of hypercalcemia has also been reported in a few patients in the burn intensive care unit. Here, the incidence of hypercalcemia in the burn unit of a single institution is reviewed. The records of all patients admitted to the burn intensive care unit over a period of 4 years of a single institution were reviewed. When looking at a select group of burn patients who have been hospitalized for more than 4 weeks, an unusually high incidence of hypercalcemia was found, especially in patients with renal failure (because of decreased renal clearance, patients with renal failure are prone to hypercalcemia if another inciting factor is present). As previously reported, the hypercalcemia in our patients was consistent with hypercalcemia caused by immobilization. We also observed that mortality correlated with higher calcium levels.

A patient with three episodes of chest wall abscesses as a result of 6 years of round-the-clock, uninterrupted (except during bathing) application of silicone gel sheets to a chest wall keloid is described. Two of the episodes occurred during hot weather. It is suggested that, in the space beneath the silicone sheet, the higher humidity and temperature, both generated as a result of prolonged sheeting, especially during hot weather, might have caused the keloid and its neighbouring skin to become soggy. This sogginess might have facilitated bacterial invasion. It is suggested that some sheeting-free time during a 24 h period might be indicated so that a keloid and its adjacent skin have the time to recover from their sheeting-induced sogginess. A sheeting-free period might especially be needed in the face of sweat accumulation beneath the silicone sheet.

Some of the highest rates of erectile dysfunction are seen in patients with renal failure, especially those on dialysis. The treatment of erectile dysfunction has been revolutionized in the last decade by the introduction of sildenafil. The literature on sildenafil in dialysis patients is here reviewed. Sildenafil seems to be both safe and effective in the treatment of sexual dysfunction in the dialysis population.

A thorough knowledge and understanding of the principles underlying the preparation and the clinical application of hemodialysates can help us provide exemplary patient care to individuals having end-stage renal disease. It is prudent to be conversant with the following: (a) how each ingredient in a dialysate works, (b) the clinical circumstances under which the concentration of an ingredient can be altered, and (c) the special situations in which unconventional ingredients can be introduced into a dialysate. The potential to enrich dialysates with appropriate ingredients (such as iron compounds) is limited only by the boundaries of our imagination.

Studies were carried out to determine whether epithelial-mesenchymal transformation (EMT), well described in renal tubular epithelial cells, also occurs in glomerular epithelial cells and whether it is reversible. To this effect, cultured glomerular epithelial cells were incubated with TGF-beta(1) and their transformation into myofibroblasts was studied. At 4 days, the cells altered their phenotype, as shown by a change in shape, an increase in intracellular staining for alpha-smooth muscle actin (alpha-SMA), a decrease in membrane staining for cytokeratin, and an increase in matrix deposition. Changing the medium after 4 days by excluding TGF-beta(1) and adding fetal bovine serum (FBS) [as a source of epidermal growth factor (EGF) and other growth factors] caused the cells to revert to their original epithelial phenotype. By contrast, when the medium was changed in the same manner after 8 days of exposure to TGF-beta(1), the cells did not revert but remained myofibroblastic. Staining the cells for expression of EGF receptor before and after exposure to TGF-beta(1) caused this receptor, originally present on the plasma membrane, to become partly intracellular after 4 days of TGF-beta(1) exposure and completely intracellular after 8 days of TGF-beta(1) exposure. Kidney sections from 2 models of renal mass reduction were stained. Loss of the epithelial marker (podocalyxin) staining and the acquisition of alpha-SMA staining was observed in the glomeruli. It is concluded that EMT takes place in glomerular epithelial cells in vivo and in vitro. In cultured glomerular epithelial cells, the process can be reversed by early, but not late intervention. It seems that TGF-beta(1) exposure progressively downregulates the EGF receptor on the membrane, rendering the cell refractory to EGF signals critical for maintaining the epithelial phenotype.

We describe a case of lipoprotein glomerulopathy, the second ever reported from the United States, in a Mexican man with a hitherto undescribed mutation in the apolipoprotein E gene (substitution of proline for arginine at position 147 [Arg147Pro]). In this patient, glomerular basement membranes showed double contours and circumferential mesangial extensions, suggesting that deposition of lipids could be injurious to endothelial cells. Immunofluorescence staining of thrombi was positive for apolipoprotein E and B. To study the reason for lipid deposition in glomeruli, we incubated normal human kidney sections with serum from the patient and a healthy control. Apolipoprotein E from the patient's serum showed binding to the glomerular capillary wall, but the control did not, suggesting enhanced binding of the mutated apolipoprotein E to glomerular capillaries. Apolipoprotein E genotyping by means of restriction endonuclease digestion of polymerase chain reaction–amplified genomic DNA showed it to be of the wild-type E3/E3.

Although transjugular renal biopsy has been used extensively in Europe, experience with its use in the United States has been limited. We report 25 patients who underwent both transjugular liver and renal biopsies in the same sitting and 4 patients who underwent only a transjugular renal biopsy. All 29 patients had both liver disease and renal abnormalities. Each patient was also believed to have a relative or absolute contraindication to a percutaneous renal biopsy (usually in the form of a bleeding abnormality). Transjugular renal biopsy yielded a quantity of tissue sufficient for diagnosis in all but 1 patient. The mean number of glomeruli obtained per biopsy was 19.4 +/- 12.2 (SD). Pathological diagnoses found were tubular injury in 5 patients, membranoproliferative glomerulonephritis in 5 patients, nephrosclerosis in 3 patients, diabetic nephropathy in 2 patients, immunoglobulin A (IgA) nephropathy in 2 patients, minimal change disease in 2 patients, end-stage renal disease in 2 patients, nonspecific changes in 1 patient, early glomerulosclerosis in 1 patient, tubular atrophy only in 1 patient, and normal renal histological characteristics in 4 patients. One patient with suspected IgA nephropathy had no histological diagnosis established because of a lack of glomeruli in the biopsy specimen. There were no instances of major bleeding from the perirenal area; however, a small perirenal hematoma was identified in 3 patients by postbiopsy computed tomography or sonography. Thus, based on our experience, transjugular renal biopsy appears to be a safe and effective procedure for establishing a histological diagnosis and is an attractive alternative biopsy method for patients with advanced liver disease and contraindications to conventional percutaneous renal biopsy.