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Kidney disease in primary Sjögren's disease

Kidney disease in primary Sjögren's disease
Literature review current through: Jan 2024.
This topic last updated: Aug 10, 2023.

INTRODUCTION — Primary Sjögren's disease (PSjD) is typically associated with a lymphocytic and plasmacytic infiltrate in the salivary, parotid, and lacrimal glands, leading to a sicca syndrome. This immune process can also affect nonexocrine organs, including the kidneys, producing a tubulointerstitial nephritis and defects in tubular function. Less commonly, a variety of glomerular diseases may also occur in association with PSjD.

The kidney manifestations of PSjD will be reviewed here. General issues related to PSjD and its diagnosis and pathogenesis are discussed separately:

(See "Clinical manifestations of Sjögren’s disease: Extraglandular disease".)

(See "Diagnosis and classification of Sjögren’s disease".)

(See "Pathogenesis of Sjögren’s disease".)

EPIDEMIOLOGY — The reported prevalence of kidney involvement in PSjD varies widely, ranging from 1 to 33 percent [1-5]. Most studies observed kidney manifestations in approximately 5 to 14 percent of patients with PSjD [4]; however, registry studies and population-based kidney biopsy studies (which may not account for patients with less severe kidney disease) have generally reported lower rates of kidney involvement [6,7], while studies that assess for sometimes subtle kidney function abnormalities (eg, partial urinary concentration and acidification defects) have reported higher rates [3].

Several studies have examined the relative prevalence of the various kidney lesions related to PSjD. The most common manifestations are interstitial nephritis and cryoglobulinemia-related membranoproliferative glomerulonephritis (MPGN) [5,8,9]. In one study that reported kidney biopsy results from 95 patients with PSjD and kidney disease, the predominant finding was tubulointerstitial nephritis in 73 patients (77 percent) and glomerular disease in 22 patients (23 percent) [9]. Of the 22 patients with glomerular disease, 8 (36 percent) had MPGN attributed to cryoglobulinemia, and the remainder had a variety of other glomerulopathies.

PATHOGENESIS — The pathogenesis of inflammation that leads to tubulointerstitial nephritis in PSjD and the etiology of mixed cryoglobulins (types II and III) that results in MPGN are discussed elsewhere. (See "Pathogenesis of Sjögren’s disease" and "Overview of cryoglobulins and cryoglobulinemia", section on 'Etiopathogenesis'.)

The defects in renal tubular function that lead to acid-base and electrolyte abnormalities in patients with PSjD (most commonly distal renal tubular acidosis [RTA], arginine vasopressin resistance [previously called nephrogenic diabetes insipidus], and hypokalemia) generally occur in conjunction with tubulointerstitial nephritis [3,5,10]; however, the precise mechanisms by which tubular inflammation/injury in PSjD may lead to specific impairments in tubular function are incompletely understood. In several patients with distal RTA and tubulitis on kidney biopsy, immunocytochemical analysis showed complete absence of the H-ATPase pump in the intercalated cells in the collecting tubules that is largely responsible for distal proton secretion [11,12], though how immune injury may cause the loss of H-ATPase remains unknown. In some patients with PSjD who have hypokalemia without RTA, the primary defect is thought to be urinary sodium wasting due to tubular injury [13]. Increased sodium delivery to the potassium secretory site in the collecting tubules and enhanced aldosterone release due to volume depletion leads to urinary potassium wasting and potentially severe hypokalemia.

Autoantibodies may underlie the acid-base and electrolyte abnormalities in some patients with PSjD. High titers of an autoantibody directed against carbonic anhydrase II have been reported in some patients with PSjD and distal RTA; inhibition of this enzyme would result in the generation within the cell of fewer hydrogen ions available for secretion [14]. In one patient with PSjD and hypokalemia due to urinary sodium wasting, a circulating autoantibody directed against the sodium-chloride cotransporter (NCCT) was identified [15].

CLINICAL PRESENTATIONS

Progressive chronic kidney disease — Chronic kidney disease (CKD) due to tubulointerstitial nephritis is the most common kidney manifestation of PSjD [6,9].

The clinical presentation of PSjD-associated tubulointerstitial nephritis may be subtle, asymptomatic, and detectable only by laboratory testing. Clinical manifestations include CKD of variable severity, a relatively benign urinalysis, and, frequently, abnormalities in tubular function such as distal (type 1) renal tubular acidosis (RTA), the Fanconi syndrome, arginine vasopressin resistance, and hypokalemia [10-13,16-19]. Less commonly, interstitial nephritis presents with subacute kidney injury [8].

Interstitial nephritis may be diagnosed before, at the same time, or after the diagnosis of PSjD, and may be identified after CKD has progressed to a moderate or even advanced degree. Because most studies of PSjD and kidney disease are small and/or combine patients with multiple types of kidney abnormalities, generalizations about the clinical characteristics of PSjD-associated interstitial nephritis are difficult to formulate. However, one of the largest kidney biopsy studies of PSjD included 95 patients, 73 of whom had tubulointerstitial nephritis, and reported the following [9]:

Most patients were diagnosed with kidney disease at the same time (58 percent) or before (11 percent) they were diagnosed with PSjD.

In 18 percent of patients, isolated electrolyte disturbances indicative of tubular dysfunction were the initial kidney manifestation of PSjD.

Most patients (68 percent) with interstitial nephritis had evidence of substantial chronicity on kidney biopsy (ie, interstitial fibrosis ≥25 percent).

The mean estimated glomerular filtration rate (eGFR) of patients with interstitial nephritis at presentation was 35 mL/min/1.73 m2.

The urinary manifestations of interstitial nephritis are relatively nonspecific. The urinalysis is either normal or shows only sterile pyuria or mild proteinuria. In 13 patients with biopsy-proven PSjD-associated interstitial nephritis, none met criteria for an active urine sediment [5]. In 64 patients with interstitial nephritis attributed to PSjD who had available 24-hour urine collections, the median urinary protein excretion was 500 mg per day [9].

Acid-base or electrolyte abnormalities — The defects in renal tubular function that lead to acid-base and electrolyte abnormalities in patients with PSjD (most commonly distal RTA, arginine vasopressin resistance, and hypokalemia) generally occur in association with tubulointerstitial nephritis [3,5,10]. However, some patients with these abnormalities and PSjD-related interstitial nephritis have a normal or near-normal eGFR [3,5]. (See 'Progressive chronic kidney disease' above.)

Distal renal tubular acidosis — A defect in distal acidification occurs in up to 25 percent of patients with PSjD [16,18]. The associated metabolic acidosis is usually mild, but some patients present with a plasma bicarbonate concentration below 10 mEq/L and a plasma potassium concentration below 2 mEq/L due to concurrent urinary potassium wasting. Muscle paralysis and respiratory arrest have been reported as consequences of the severe hypokalemia [16,18,20]. (See "Overview and pathophysiology of renal tubular acidosis and the effect on potassium balance".)

Patients may present with a distal RTA without a prior diagnosis of PSjD [16]. In a review of case reports and series of patients with PSjD and presumptive RTA, approximately 8 percent of patients had a diagnosis of PSjD at presentation [20]. It is therefore important to consider the diagnosis of PSjD in any adult with otherwise unexplained distal RTA. (See "Etiology and diagnosis of distal (type 1) and proximal (type 2) renal tubular acidosis".)

Urinary concentration defects — Arginine vasopressin resistance leading to polyuria and polydipsia is another potential manifestation of impaired tubular function in PSjD [10]. In one study of 60 patients with PSjD, a water deprivation test was performed in patients who had abnormally low values of morning urine osmolality [3]. Urinary concentration defects were observed in 10 of 48 (21 percent) tested patients.

Patients who present with arginine vasopressin resistance due to PSjD may not have characteristic symptoms of PSjD. It is therefore important to exclude PSjD in any adult with symptomatic arginine vasopressin resistance who does not have the two most common causes of this disorder: chronic lithium ingestion or hypercalcemia. (See "Arginine vasopressin resistance (nephrogenic diabetes insipidus): Clinical manifestations and causes".)

Hypokalemia without renal tubular acidosis — Some patients with PSjD may have hypokalemia without RTA. In such patients, the primary defect appears to be urinary sodium wasting due to tubular injury. These patients can acidify the urine normally and do not have metabolic acidosis [13]. (See 'Pathogenesis' above.)

The clinical features associated with this phenotype are similar to those of Gitelman syndrome, an inherited hypokalemic salt-losing tubulopathy. As such, PSjD is in the differential diagnosis in patients with acquired Gitelman-like syndromes [15]. (See "Bartter and Gitelman syndromes in adults: Diagnosis and management", section on 'Acquired syndromes' and "Inherited hypokalemic salt-losing tubulopathies: Pathophysiology and overview of clinical manifestations".)

Nephritic syndrome — Nephritic syndrome is a less common kidney manifestation of PSjD. Patients typically present with hematuria, proteinuria (which can sometimes be in the nephrotic range), hypertension, and varying degrees of kidney function impairment. Such patients usually have membranoproliferative glomerulonephritis (MPGN) associated with cryoglobulinemia, although other causes of glomerulonephritis have been reported.

MPGN due to cryoglobulinemia MPGN secondary to cryoglobulinemia is the most common glomerular pathology associated with PSjD, and PSjD is a major cause of non-hepatitis C–associated mixed cryoglobulinemia [21]. Studies of kidney biopsy findings in PSjD report cryoglobulinemia-associated MPGN in 5 to 30 percent of patients [3,5,6,9].

Other causes of glomerulonephritis – Less frequently, a variety of other glomerulonephritides may occur in patients with PSjD, including antineutrophil cytoplasmic autoantibody (ANCA)-associated pauci-immune glomerulonephritis [8,22,23] and immunoglobulin (Ig) A nephropathy [3,5,8].

Uncommon presentations

Nephrotic syndrome Nephrotic syndrome is uncommon in patients with PSjD and kidney disease. Studies of kidney biopsy findings in PSjD generally report membranous nephropathy in less than 10 percent of patients [3,5,6,9]. The possible etiologic relationship between PSjD and membranous nephropathy is unclear. Other protein-losing nephropathies, such as focal and segmental glomerulosclerosis and minimal change disease, also have been reported in patients with PSjD [5,6,9,24].

Kidney mass – Patients with PSjD may develop a kidney lymphoma that presents as a kidney mass. Although PSjD is associated with an increased risk of non-Hodgkin lymphoma [25], the occurrence of kidney lymphoma is uncommon [4].

DIAGNOSIS

When to suspect Sjögren-related kidney disease — Sjogren-related kidney disease should be suspected in any patient with an established diagnosis or characteristic features of PSjD who presents with any of the following:

Chronic kidney disease (CKD) or subacute kidney injury (see 'Progressive chronic kidney disease' above)

Unexplained metabolic acidosis (see 'Distal renal tubular acidosis' above)

Polyuria and polydipsia (see 'Urinary concentration defects' above)

Unexplained hypokalemia (see 'Hypokalemia without renal tubular acidosis' above)

Urinary findings suggestive of glomerulonephritis (ie, hematuria and proteinuria) (see 'Nephritic syndrome' above)

Evaluation — For patients with suspected Sjogren-related kidney disease, the evaluation is guided by the clinical presentation:

CKD or subacute kidney injury – Patients presenting with CKD or subacute kidney injury should be thoroughly evaluated for other potential causes using the same diagnostic approach as that for patients without PSjD. (See "Chronic kidney disease (newly identified): Clinical presentation and diagnostic approach in adults" and "Diagnostic approach to adult patients with subacute kidney injury in an outpatient setting".)

In patients with PSjD who have impaired/worsening kidney function without an identified cause, a kidney biopsy is usually performed to define the nature of kidney involvement. However, the most common Sjogren-related kidney lesion, tubulointerstitial nephritis, is not specific to PSjD. As such, the diagnosis of PSjD-associated interstitial nephritis requires three elements:

A diagnosis of PSjD (see "Diagnosis and classification of Sjögren’s disease")

Interstitial nephritis demonstrated by kidney biopsy (see "Clinical manifestations and diagnosis of acute interstitial nephritis", section on 'Histology')

Exclusion of other etiologies of interstitial nephritis (see "Clinical manifestations and diagnosis of acute interstitial nephritis", section on 'Establishing the cause')

The tubulointerstitial nephritis in PSjD is characterized histologically by an interstitial infiltrate that can invade and damage the tubules [3,19,26]. In some cases, granuloma formation is seen [6,27]. More chronic disease is associated with tubular atrophy and interstitial fibrosis. The glomeruli are usually normal.

Among patients with interstitial nephritis who do not have an established diagnosis of PSjD, other conditions that must be considered include IgG4-related disease, sarcoidosis, and tubulointerstitial nephritis with uveitis (TINU). These diseases may present with clinical features that mimic PSjD. (See "Diagnosis and classification of Sjögren’s disease", section on 'Differential diagnosis' and "Tubulointerstitial nephritis and uveitis (TINU syndrome)", section on 'Differential diagnosis'.)

Acid-base or electrolyte abnormalities – The diagnoses of renal tubular acidosis (RTA) and arginine vasopressin resistance are discussed in detail elsewhere. (See "Etiology and diagnosis of distal (type 1) and proximal (type 2) renal tubular acidosis" and "Evaluation of patients with polyuria".)

Nephritic syndrome Patients presenting with features of the nephritic syndrome should be evaluated for glomerulonephritis, which generally involves laboratory testing and, in many cases, a kidney biopsy to obtain a definitive diagnosis. Measurement of serum cryoglobulins and testing for hepatitis C should be included as part of the evaluation. The approach to the evaluation of glomerulonephritis is presented separately. (See "Glomerular disease: Evaluation and differential diagnosis in adults", section on 'Evaluation of glomerulonephritis' and "Mixed cryoglobulinemia syndrome: Clinical manifestations and diagnosis", section on 'Testing for cryoglobulins'.)

MANAGEMENT

Tubulointerstitial nephritis — The treatment of PSjD-associated interstitial nephritis is discussed below. The general management of patients with chronic kidney disease (CKD) or acute kidney injury (AKI), regardless of cause, is discussed elsewhere. (See "Overview of the management of chronic kidney disease in adults" and "Overview of the management of acute kidney injury (AKI) in adults".)

The optimal therapy for patients with PSjD-associated interstitial nephritis is unclear. For most patients with active tubulointerstitial nephritis, we suggest treatment with glucocorticoids. We generally do not administer glucocorticoids to patients with interstitial nephritis who have severe interstitial fibrosis on kidney biopsy (ie, >50 to 75 percent), since the risk of immunosuppressive therapy in such patients typically outweighs the benefits. Infrequently, however, some patients with severe fibrosis on biopsy may lack characteristic ultrasound findings of diffuse kidney scarring (ie, relatively small, echogenic kidneys), have relatively well-preserved kidney function documented in the preceding three to six months, and/or present with only moderate decrements in estimated glomerular filtration rate (eGFR). One or more of these features raise the possibility of sampling error on biopsy; in such cases, the decision to treat active interstitial nephritis with glucocorticoids is determined by shared decision-making and is based on the individual patient's comorbidities and risk tolerance.

High-quality data do not exist to guide the dosing or course of glucocorticoid therapy. We initially treat with high-dose prednisone 1 mg/kg per day (maximum daily dose of 60 mg) for four to six weeks. Our subsequent treatment depends on the response to initial therapy:

If kidney function stabilizes or improves, we taper prednisone over the next six to eight weeks to complete an approximately three-month long course of immunosuppressive therapy. If kidney function worsens during the glucocorticoid taper or shortly after stopping glucocorticoid therapy, we restart high-dose prednisone and add either mycophenolate mofetil (MMF; 0.5 to 1 g twice daily) or azathioprine (AZA; 1 to 1.5 mg/kg per day) as a glucocorticoid-sparing agent to permit a glucocorticoid taper and eventual discontinuation of glucocorticoids. A reasonable duration of MMF or AZA is 12 months.

If kidney function worsens despite initial therapy, MMF (1 g twice daily) or AZA (1.5 mg/kg per day) may be added, and high-dose prednisone continued for another two to three weeks. If kidney function subsequently stabilizes or improves, the prednisone dose can then be tapered over the next six to eight weeks and MMF or AZA continued for a prolonged period (eg, 12 months). However, if kidney function continues to worsen despite the addition of MMF or AZA to high-dose prednisone, the risks of ongoing immunosuppressive therapy likely outweigh the benefits. In such patients, MMF or AZA can be stopped and the prednisone rapidly tapered.

Although data are sparse, MMF with or without reduced dose glucocorticoids also has been used as initial therapy for PSjD-associated interstitial nephritis. [28,29].

Evidence to support the use of immunosuppressive medications for the treatment of PSjD-associated interstitial nephritis is limited to case reports and series [6,9,28-30]. In one of the largest case series, 64 patients with PSjD and isolated interstitial nephritis were treated with immunosuppressive therapy and had available baseline and follow-up serum creatinine data [9]. Salient findings include the following:

Immunosuppressive therapy was associated with stabilization or slight improvement in kidney function. The mean eGFR was 35 mL/min/1.73 m2 at baseline and approximately 43 mL/min/1.73 m2 at 6 and 12 months of follow-up.

Half the patients (n = 32) had a treatment-associated increase in eGFR of ≥20 percent at 12 months of follow-up.

Patients treated with glucocorticoid monotherapy (n = 43) had kidney outcomes similar to those of patients treated with the combination of glucocorticoids plus either rituximab (n = 10), AZA (n = 6), or MMF (n = 5).

Although the availability of kidney function data after 12 months of treatment was limited, only four patients progressed to end-stage kidney disease at a median follow-up of five years.

Treatment response in this study may have been limited by the degree of fibrosis on kidney biopsy; of the 31 patients with interstitial nephritis who had available fibrosis data, over two-thirds had interstitial fibrosis >25 percent.

Acid-base or electrolyte abnormalities — The management of acid-base and electrolyte abnormalities in patients with PSjD is the same as that for patients without PSjD and is discussed separately:

Distal renal tubular acidosis (see "Treatment of distal (type 1) and proximal (type 2) renal tubular acidosis")

Arginine vasopressin resistance (see "Arginine vasopressin resistance (nephrogenic diabetes insipidus): Treatment")

Hypokalemia (see "Clinical manifestations and treatment of hypokalemia in adults")

The role of immunosuppression in patients with severe manifestations of PSjD-related distal RTA (eg, refractory calcium phosphate stone disease) who have a preserved eGFR is unclear. In general, we do not subject such patients to the risks of kidney biopsy or immunosuppressive therapy. However, we monitor such patients and typically perform a kidney biopsy if eGFR worsens; PSjD-associated interstitial nephritis in conjunction with impaired/worsening kidney function is an indication for immunosuppressive therapy. (See 'Tubulointerstitial nephritis' above.)

The management of distal RTA-associated urinary stone disease is discussed in detail elsewhere. (See "Nephrolithiasis in renal tubular acidosis".)

Membranoproliferative glomerulonephritis secondary to cryoglobulinemia — Patients with PSjD and biopsy-proven MPGN due to cryoglobulinemia should be treated using the same approach as that for patients with mixed cryoglobulinemia syndrome who have glomerulonephritis. This is discussed in detail separately. (See "Mixed cryoglobulinemia syndrome: Treatment and prognosis".)

PROGNOSIS — Long-term outcome data in patients with PSjD-associated kidney disease are sparse. Compared with patients who have predominantly tubulointerstitial involvement, patients with predominantly glomerular disease may be less likely to develop end-stage kidney disease but may have higher rates of lymphoma and mortality [5].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Chronic kidney disease in adults" and "Society guideline links: Sjögren's disease".)

SUMMARY AND RECOMMENDATIONS

Epidemiology – The reported prevalence of kidney involvement in patients with primary Sjögren's disease (PSjD) varies widely, ranging from approximately 1 to 33 percent. This variability is due in part to different definitions of kidney involvement. (See 'Epidemiology' above.)

Clinical presentations

Progressive chronic kidney disease – Chronic kidney disease (CKD) due to tubulointerstitial nephritis is the most common kidney manifestation of PSjD. Patients with PSjD-associated interstitial nephritis present with CKD of variable severity, a relatively benign urinalysis, and, frequently, abnormalities in tubular function such as distal (type 1) renal tubular acidosis (RTA), arginine vasopressin resistance (previously called nephrogenic diabetes insipidus), and hypokalemia. Less commonly, interstitial nephritis presents with subacute kidney injury. (See 'Progressive chronic kidney disease' above.)

Acid-base or electrolyte abnormalities – The defects in renal tubular function that lead to acid-base and electrolyte abnormalities in patients with PSjD generally occur in association with tubulointerstitial nephritis. However, some patients with these abnormalities and PSjD-related interstitial nephritis have a normal or near-normal estimated glomerular filtration rate (eGFR). (See 'Acid-base or electrolyte abnormalities' above.)

-Distal renal tubular acidosis – A defect in distal acidification occurs in up to 25 percent of patients with PSjD. The associated metabolic acidosis is usually mild, but some patients present with a plasma bicarbonate concentration below 10 mEq/L and a plasma potassium concentration below 2 mEq/L due to concurrent urinary potassium wasting. Because patients may present with a distal RTA without a prior diagnosis of PSjD, it is important to consider the diagnosis of PSjD in any adult with otherwise unexplained distal RTA. (See 'Distal renal tubular acidosis' above.)

-Urinary concentration defects – Arginine vasopressin resistance leading to polyuria and polydipsia is another potential manifestation of impaired tubular function in PSjD. PSjD should be excluded in any adult with symptomatic arginine vasopressin resistance who does not have the two most common causes of this disorder: chronic lithium ingestion or hypercalcemia. (See 'Urinary concentration defects' above.)

-Hypokalemia without renal tubular acidosis – Some patients with PSjD may have hypokalemia without RTA. In such patients, the primary defect appears to be urinary sodium wasting due to tubular injury. (See 'Hypokalemia without renal tubular acidosis' above.)

Nephritic syndrome – Nephritic syndrome is a less common kidney manifestation of PSjD. Patients typically present with hematuria, proteinuria (which can sometimes be in the nephrotic range), hypertension, and varying degrees of kidney function impairment. Such patients usually have membranoproliferative glomerulonephritis (MPGN) associated with cryoglobulinemia. (See 'Nephritic syndrome' above.)

Diagnosis – For patients with suspected Sjogren-related kidney disease, the evaluation is guided by the clinical presentation. (See 'Diagnosis' above.)

Management

Tubulointerstitial nephritis – For most patients with active tubulointerstitial nephritis due to PSjD, we suggest treatment with glucocorticoids rather than no immunosuppressive therapy or other immunosuppressive agents (Grade 2C). We use mycophenolate mofetil (MMF) and azathioprine (AZA) in select patients. (See 'Tubulointerstitial nephritis' above.)

Acid-base or electrolyte abnormalities – The management of acid-base and electrolyte abnormalities in patients with PSjD is the same as that for patients without PSjD. (See 'Acid-base or electrolyte abnormalities' above.)

MPGN secondary to cryoglobulinemia – Patients with PSjD and biopsy-proven MPGN due to cryoglobulinemia should be treated using the same approach as that for patients with mixed cryoglobulinemia syndrome who have glomerulonephritis. (See "Mixed cryoglobulinemia syndrome: Treatment and prognosis".)

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Topic 7187 Version 40.0

References

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